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6. Cardiac metabolism as a driver and therapeutic target of myocardial infarction

Author

Zuurbier, C.J. Bertrand, L. Beauloye, C.R. Andreadou, I. Ruiz-Meana, M. Jespersen, N.R. Kula-Alwar, D. Prag, H.A. Eric Botker, H. Dambrova, M. Montessuit, C. Kaambre, T. Liepinsh, E. Brookes, P.S. Krieg, T.

Abstract

Reducing infarct size during a cardiac ischaemic-reperfusion episode is still of paramount importance, because the extension of myocardial necrosis is an important risk factor for developing heart failure. Cardiac ischaemia-reperfusion injury (IRI) is in principle a metabolic pathology as it is caused by abruptly halted metabolism during the ischaemic episode and exacerbated by sudden restart of specific metabolic pathways at reperfusion. It should therefore not come as a surprise that therapy directed at metabolic pathways can modulate IRI. Here, we summarize the current knowledge of important metabolic pathways as therapeutic targets to combat cardiac IRI. Activating metabolic pathways such as glycolysis (eg AMPK activators), glucose oxidation (activating pyruvate dehydrogenase complex), ketone oxidation (increasing ketone plasma levels), hexosamine biosynthesis pathway (O-GlcNAcylation; administration of glucosamine/glutamine) and deacetylation (activating sirtuins 1 or 3; administration of NAD+-boosting compounds) all seem to hold promise to reduce acute IRI. In contrast, some metabolic pathways may offer protection through diminished activity. These pathways comprise the malate-aspartate shuttle (in need of novel specific reversible inhibitors), mitochondrial oxygen consumption, fatty acid oxidation (CD36 inhibitors, malonyl-CoA decarboxylase inhibitors) and mitochondrial succinate metabolism (malonate). Additionally, protecting the cristae structure of the mitochondria during IR, by maintaining the association of hexokinase II or creatine kinase with mitochondria, or inhibiting destabilization of FOF1-ATPase dimers, prevents mitochondrial damage and thereby reduces cardiac IRI. Currently, the most promising and druggable metabolic therapy against cardiac IRI seems to be the singular or combined targeting of glycolysis, O-GlcNAcylation and metabolism of ketones, fatty acids and succinate. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd

Published
2020

9. Protection of reoxygenated cardiomyocytes against osmotic fragility by nitric oxide donors

Author

Schluter, K.D., Jakob, G., Ruiz-Meana, M., Garcia-Dorado, D., and Piper, H.M.

Subjects
Hypoxia -- Physiological aspects, Heart cells -- Research, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

Increased osmotic fragility of isolated adult rat cardiomyocytes can be attenuated at the onset of reoxygenation by interventions of nitric oxide donors or a lipophilic antilipid peroxidant. Reoxygenation causes enzyme loss if combined with osmotic stress. The protective effects of nitric oxide donors and antilipid peroxidant diphenylphenylenediamine are independent of influence on reoxygenation-induced hypercontracture. Their effect is also independent of any guanosine 3',5'-cyclic monophosphate mediation.

Published
1996

11. Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

Author

Bøtker, H.E. Hausenloy, D. Andreadou, I. Antonucci, S. Boengler, K. Davidson, S.M. Deshwal, S. Devaux, Y. Di Lisa, F. Di Sante, M. Efentakis, P. Femminò, S. García-Dorado, D. Giricz, Z. Ibanez, B. Iliodromitis, E. Kaludercic, N. Kleinbongard, P. Neuhäuser, M. Ovize, M. Pagliaro, P. Rahbek-Schmidt, M. Ruiz-Meana, M. Schlüter, K.-D. Schulz, R. Skyschally, A. Wilder, C. Yellon, D.M. Ferdinandy, P. Heusch, G.

Published
2018

13. Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery

Author

Hausenloy D., Barrabes J., Bøtker H., Davidson S., Di Lisa F., Downey J., Engstrom T., Ferdinandy P., Carbrera-Fuentes H., Heusch G., Ibanez B., Iliodromitis E., Inserte J., Jennings R., Kalia N., Kharbanda R., Lecour S., Marber M., Miura T., Ovize M., Perez-Pinzon M., Piper H., Przyklenk K., Schmidt M., Redington A., Ruiz-Meana M., Vilahur G., Vinten-Johansen J., Yellon D., and Garcia-Dorado D.

Subjects
Myocardial reperfusion injury, RISK and SAFE pathway, Ischaemic conditioning, Cardioprotection, Mitochondria
Abstract

© 2016, The Author(s).To commemorate the auspicious occasion of the 30th anniversary of IPC, leading pioneers in the field of cardioprotection gathered in Barcelona in May 2016 to review and discuss the history of IPC, its evolution to IPost and RIC, myocardial reperfusion injury as a therapeutic target, and future targets and strategies for cardioprotection. This article provides an overview of the major topics discussed at this special meeting and underscores the huge importance and impact, the discovery of IPC has made in the field of cardiovascular research.

Published
2016

14. Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery

Author

Hausenloy, D.J. Barrabes, J.A. Bøtker, H.E. Davidson, S.M. Di Lisa, F. Downey, J. Engstrom, T. Ferdinandy, P. Carbrera-Fuentes, H.A. Heusch, G. Ibanez, B. Iliodromitis, E.K. Inserte, J. Jennings, R. Kalia, N. Kharbanda, R. Lecour, S. Marber, M. Miura, T. Ovize, M. Perez-Pinzon, M.A. Piper, H.M. Przyklenk, K. Schmidt, M.R. Redington, A. Ruiz-Meana, M. Vilahur, G. Vinten-Johansen, J. Yellon, D.M. Garcia-Dorado, D.

Abstract

To commemorate the auspicious occasion of the 30th anniversary of IPC, leading pioneers in the field of cardioprotection gathered in Barcelona in May 2016 to review and discuss the history of IPC, its evolution to IPost and RIC, myocardial reperfusion injury as a therapeutic target, and future targets and strategies for cardioprotection. This article provides an overview of the major topics discussed at this special meeting and underscores the huge importance and impact, the discovery of IPC has made in the field of cardiovascular research. © 2016, The Author(s).

Published
2016

20. ESC Working Group Cellular Biology of the Heart: Position Paper: improving the preclinical assessment of novel cardioprotective therapies

Author

Lecour, S., primary, Botker, H. E., additional, Condorelli, G., additional, Davidson, S. M., additional, Garcia-Dorado, D., additional, Engel, F. B., additional, Ferdinandy, P., additional, Heusch, G., additional, Madonna, R., additional, Ovize, M., additional, Ruiz-Meana, M., additional, Schulz, R., additional, Sluijter, J. P. G., additional, Van Laake, L. W., additional, Yellon, D. M., additional, and Hausenloy, D. J., additional

Published
2014
Full Text
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28. Sunday, 18 July 2010

Author

Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., additional, Piccini, I., additional, Fortmueller, L., additional, Kuhlmann, M., additional, Schaefers, M., additional, Carmeliet, P., additional, Kirchhof, P., additional, Fabritz, L., additional, Sanchez, J., additional, Rodriguez-Sinovas, A., additional, Agullo, E., additional, Garcia-Dorado, D., additional, Lymperopoulos, A., additional, Rengo, G., additional, Gao, E., additional, Zincarelli, C., additional, Koch, W., additional, Morgan, P., additional, Diez, A., additional, Perez, N., additional, Cingolani, H., additional, Zahradnikova, A., additional, Polakova, E., additional, Zahradnik, I., additional, Fluschnik, N., additional, Sossalla, S., additional, Ort, K., additional, Neef, S., additional, Hasenfuss, G., additional, Maier, L., additional, Weinert, S., additional, Poitz, D., additional, Herold, J., additional, Schmeisser, A., additional, Strasser, J., additional, Braun-Dullaeus, R., additional, Nazari-Jahantigh, M., additional, Weber, C., additional, Schober, A., additional, Leuner, A., additional, Eichhorn, B., additional, Ravens, U., additional, Morawietz, H., additional, Babes, E., additional, Babes, V., additional, Popescu, M., additional, Ardelean, A., additional, Rus, M., additional, Bustea, C., additional, Gwozdz, P., additional, Csanyi, G., additional, Luzak, B., additional, Gajda, M., additional, Mateuszuk, L., additional, Chmura-Skirlinska, A., additional, Watala, C., additional, Chlopicki, S., additional, Kierzkowska, I., additional, Sulicka, J., additional, Kwater, A., additional, Strach, M., additional, Surdacki, A., additional, Siedlar, M., additional, Grodzicki, T., additional, Olieslagers, S., additional, Pardali, L., additional, Tchaikovski, V., additional, Ten Dijke, P., additional, Waltenberger, J., additional, Renner, M., additional, Redwan, B., additional, Winter, M., additional, Panzenboeck, A., additional, Jakowitsch, J., additional, Sadushi-Kolici, R., additional, Bonderman, D., additional, Lang, I., additional, Toso, A., additional, Tanini, L., additional, Pizzetti, T., additional, Leoncini, M., additional, Maioli, M., additional, Tedeschi, D., additional, Oliviero, C., additional, Bellandi, F., additional, Casprini, P., additional, Amato, M., additional, Molins, B., additional, Pena, E., additional, Badimon, L., additional, Ferreiro Gutierrez, J., additional, Ueno, M., additional, Alissa, R., additional, Dharmashankar, K., additional, Capodanno, D., additional, Desai, B., additional, Bass, T., additional, Angiolillo, D., additional, Chabielska, E., additional, Gromotowicz, A., additional, Szemraj, J., additional, Stankiewicz, A., additional, Zakrzeska, A., additional, Mohammed, S., additional, Molla, F., additional, Soldo, A., additional, Russo, I., additional, Germano, G., additional, Balconi, G., additional, Staszewsky, L., additional, Latini, R., additional, Lynch, F., additional, Austin, C., additional, Prendergast, B., additional, Keenan, D., additional, Malik, R., additional, Izzard, A., additional, Heagerty, A., additional, Czikora, A., additional, Lizanecz, E., additional, Rutkai, I., additional, Boczan, J., additional, Porszasz, R., additional, Papp, Z., additional, Edes, I., additional, Toth, A., additional, Colantuoni, A., additional, Vagnani, S., additional, Lapi, D., additional, Maroz-Vadalazhskaya, N., additional, Koslov, I., additional, Shumavetz, V., additional, Glibovskaya, T., additional, Ostrovskiy, Y., additional, Koutsiaris, A., additional, Tachmitzi, S., additional, Kotoula, M., additional, Giannoukas, A., additional, Tsironi, E., additional, Darago, A., additional, Orosz, P., additional, Megyesi, Z., additional, Schudeja, S., additional, Matschke, K., additional, Deussen, A., additional, Castro, M., additional, Cena, J., additional, Walsh, M., additional, Schulz, R., additional, Poddar, K., additional, Rha, S., additional, Ramasamy, S., additional, Park, J., additional, Choi, C., additional, Seo, H., additional, Park, C., additional, Oh, D., additional, Almeida, J., additional, Pimenta, S., additional, Bernardes, J., additional, Machado, J., additional, Sabatasso, S., additional, Laissue, J., additional, Hlushchuk, R., additional, Brauer-Krisch, E., additional, Bravin, A., additional, Blattmann, H., additional, Michaud, K., additional, Djonov, V., additional, Hirschberg, K., additional, Tarcea, V., additional, Pali, S., additional, Korkmaz, S., additional, Loganathan, S., additional, Merkely, B., additional, Karck, M., additional, Szabo, G., additional, Pagliani, L., additional, Faggin, E., additional, Rattazzi, M., additional, Puato, M., additional, Presta, M., additional, Grego, F., additional, Deriu, G., additional, Pauletto, P., additional, Kaiser, R., additional, Albrecht, K., additional, Schgoer, W., additional, Theurl, M., additional, Beer, A., additional, Wiedemann, D., additional, Steger, C., additional, Bonaros, N., additional, Kirchmair, R., additional, Kharlamov, A., additional, Cabaravdic, M., additional, Breuss, J., additional, Uhrin, P., additional, Binder, B., additional, Fiordaliso, F., additional, Maggioni, M., additional, Biondi, A., additional, Masson, S., additional, Cervo, L., additional, Francke, A., additional, Soenke, W., additional, Strasser, R., additional, Hecht, N., additional, Vajkoczy, P., additional, Woitzik, J., additional, Hackbusch, D., additional, Gatzke, N., additional, Duelsner, A., additional, Tsuprykov, O., additional, Slavic, S., additional, Buschmann, I., additional, Kappert, K., additional, Massaro, M., additional, Scoditti, E., additional, Carluccio, M., additional, Storelli, C., additional, Distante, A., additional, De Caterina, R., additional, Barandi, L., additional, Harmati, G., additional, Simko, J., additional, Horvath, B., additional, Szentandrassy, N., additional, Banyasz, T., additional, Magyar, J., additional, Nanasi, P., additional, Kaya, A., additional, Uzunhasan, I., additional, Yildiz, A., additional, Yigit, Z., additional, Turkoglu, C., additional, Doisne, N., additional, Zannad, N., additional, Hivert, B., additional, Cosnay, P., additional, Maupoil, V., additional, Findlay, I., additional, Virag, L., additional, Kristof, A., additional, Koncz, I., additional, Szel, T., additional, Jost, N., additional, Biliczki, P., additional, Papp, J., additional, Varro, A., additional, Bukowska, A., additional, Skopp, K., additional, Hammwoehner, M., additional, Huth, C., additional, Bode-Boeger, S., additional, Goette, A., additional, Workman, A., additional, Dempster, J., additional, Marshall, G., additional, Rankin, A., additional, Revnic, C., additional, Ginghina, C., additional, Revnic, F., additional, Yakushev, S., additional, Petrushanko, I., additional, Makhro, A., additional, Segato Komniski, M., additional, Mitkevich, V., additional, Makarov, A., additional, Gassmann, M., additional, Bogdanova, A., additional, Rutkovskiy, A., additional, Mariero, L., additional, Stenslokken, K., additional, Valen, G., additional, Vaage, J., additional, Dizayee, S., additional, Kaestner, S., additional, Kuck, F., additional, Piekorz, R., additional, Hein, P., additional, Matthes, J., additional, Nurnberg, B., additional, Herzig, S., additional, Hertel, F., additional, Switalski, A., additional, Bender, K., additional, Kienitz, M.-C., additional, Pott, L., additional, Fornai, L., additional, Angelini, A., additional, Erika Amstalden Van Hove, E., additional, Fedrigo, M., additional, Heeren, R., additional, Kruse, M., additional, Pongs, O., additional, Lehmann, H., additional, Martens-Lobenhoffer, J., additional, Roehl, F., additional, Radicke, S., additional, Cotella, C., additional, Sblattero, D., additional, Schaefer, M., additional, Wettwer, E., additional, Santoro, C., additional, Seyler, C., additional, Kulzer, M., additional, Zitron, E., additional, Scholz, E., additional, Welke, F., additional, Thomas, D., additional, Karle, C., additional, Schmidt, K., additional, Dobrev, D., additional, Houshmand, N., additional, Menesi, D., additional, Cotella, D., additional, Szuts, V., additional, Puskas, L., additional, Kiss, I., additional, Deak, F., additional, Tereshchenko, S., additional, Gladyshev, M., additional, Kalachova, G., additional, Syshchik, N., additional, Gogolashvili, N., additional, Dedok, E., additional, Evert, L., additional, Wenzel, J., additional, Brandenburger, M., additional, Bogdan, R., additional, Richardt, D., additional, Reppel, M., additional, Hescheler, J., additional, Dendorfer, A., additional, Terlau, H., additional, Wiegerinck, R., additional, Galvez-Monton, C., additional, Jorge, E., additional, Martinez, R., additional, Ricart, E., additional, Cinca, J., additional, Bagavananthem Andavan, G., additional, Lemmens Gruber, R., additional, Brack, K., additional, Coote, J., additional, Ng, G., additional, Daimi, H., additional, Haj Khelil, A., additional, Neji, A., additional, Ben Hamda, K., additional, Maaoui, S., additional, Aranega, A., additional, Chibani, J., additional, Franco Jaime, D., additional, Tanko, A.-S., additional, Daniel, J.-M., additional, Bielenberg, W., additional, Stieger, P., additional, Tillmanns, H., additional, Sedding, D., additional, Fortini, C., additional, Toffoletto, B., additional, Fucili, A., additional, Beltrami, A., additional, Fiorelli, V., additional, Francolini, G., additional, Ferrari, R., additional, Beltrami, C., additional, Castellani, C., additional, Ravara, B., additional, Tavano, R., additional, Vettor, R., additional, De Coppi, P., additional, Papini, E., additional, Gunetti, M., additional, Fagioli, F., additional, Suffredini, S., additional, Sartiani, L., additional, Stillitano, F., additional, Mugelli, A., additional, Cerbai, E., additional, Krausgrill, B., additional, Halbach, M., additional, Soemantri, S., additional, Schenk, K., additional, Lange, N., additional, Saric, T., additional, Muller-Ehmsen, J., additional, Kavanagh, D., additional, Zhao, Y., additional, Yemm, A., additional, Kalia, N., additional, Wright, E., additional, Farrell, K., additional, Wallrapp, C., additional, Geigle, P., additional, Lewis, A., additional, Stratford, P., additional, Malik, N., additional, Holt, C., additional, Raths, M., additional, Zagallo, M., additional, Luni, C., additional, Serena, E., additional, Cimetta, E., additional, Zatti, S., additional, Giobbe, G., additional, Elvassore, N., additional, Zaglia, T., additional, Zambon, A., additional, Gordon, K., additional, Mioulane, M., additional, Foldes, G., additional, Ali, N., additional, Harding, S., additional, Gorbe, A., additional, Szunyog, A., additional, Varga, Z., additional, Pirity, M., additional, Rungaruniert, S., additional, Dinnyes, A., additional, Csont, T., additional, Ferdinandy, P., additional, Iqbal, A., additional, Schneider, M. D., additional, Khodjaeva, E., additional, Ibadov, R., additional, Khalikulov, K., additional, Mansurov, A., additional, Astvatsatryan, A., additional, Senan, M., additional, Nemeth, A., additional, Lenkey, Z., additional, Ajtay, Z., additional, Cziraki, A., additional, Sulyok, E., additional, Horvath, I., additional, Lobenhoffer, J., additional, Bode-Boger, S., additional, Li, J., additional, He, Y., additional, Yang, X., additional, Wang, F., additional, Xu, H., additional, Li, X., additional, Zhao, X., additional, Lin, Y., additional, Juszynski, M., additional, Ciszek, B., additional, Jablonska, A., additional, Stachurska, E., additional, Ratajska, A., additional, Atkinson, A., additional, Inada, S., additional, Sleiman, R., additional, Zhang, H., additional, Boyett, M., additional, Dobrzynski, H., additional, Fedorenko, O., additional, Hao, G., additional, Yanni, J., additional, Buckley, D., additional, Anderson, R., additional, Ma, Y., additional, Ma, X., additional, Hu, Y., additional, Yang, Y., additional, Huang, D., additional, Liu, F., additional, Huang, Y., additional, Liu, C., additional, Jedrzejczyk, T., additional, Balwicki, L., additional, Wierucki, L., additional, Zdrojewski, T., additional, Agarkova, I., additional, Vogel, J., additional, Korybalska, K., additional, Pyda, M., additional, Witowski, J., additional, Ibatov, A., additional, Sozmen, N., additional, Seymen, A., additional, Tuncay, E., additional, Turan, B., additional, Chen, B., additional, Houston-Feenstra, L., additional, Chiong, J. R., additional, Jutzy, K., additional, Furundzija, V., additional, Kaufmann, J., additional, Meyborg, H., additional, Fleck, E., additional, Stawowy, P., additional, Ksiezycka-Majczynska, E., additional, Lubiszewska, B., additional, Kruk, M., additional, Kurjata, P., additional, Ruzyllo, W., additional, Driesen, R., additional, Coenen, T., additional, Fagard, R., additional, Sipido, K., additional, Petrov, V., additional, Aksentijevic, D., additional, Lygate, C., additional, Makinen, K., additional, Sebag-Montefiore, L., additional, Medway, D., additional, Schneider, J., additional, Neubauer, S., additional, Gasser, R., additional, Holzwart, E., additional, Rainer, P., additional, Von Lewinski, D., additional, Maechler, H., additional, Gasser, S., additional, Roessl, U., additional, Pieske, B., additional, Krueger, J., additional, Kintscher, U., additional, Podramagi, T., additional, Paju, K., additional, Piirsoo, A., additional, Roosimaa, M., additional, Kadaja, L., additional, Orlova, E., additional, Ruusalepp, A., additional, Seppet, E., additional, Auquier, J., additional, Ginion, A., additional, Hue, L., additional, Horman, S., additional, Beauloye, C., additional, Vanoverschelde, J., additional, Bertrand, L., additional, Fekete, V., additional, Zvara, A., additional, Pipis, J., additional, Konya, C., additional, Csonka, C., additional, Kraigher-Krainer, E., additional, Von Lewinksi, D., additional, Gonzalez-Loyola, A., additional, Barba, I., additional, Fernandez-Sanz, C., additional, Ruiz-Meana, M., additional, Forteza, M., additional, Bodi Peris, V., additional, Monleon, D., additional, Mainar, L., additional, Morales, J., additional, Moratal, D., additional, Trapero, I., additional, Chorro, F., additional, Leszek, P., additional, Sochanowicz, B., additional, Szperl, M., additional, Kolsut, P., additional, Piotrowski, W., additional, Rywik, T., additional, Danko, B., additional, Kruszewski, M., additional, Stanley, W., additional, Khairallah, R., additional, Khanna, N., additional, O'shea, K., additional, Kristian, T., additional, Hecker, P., additional, Des Rosiers, R., additional, Fiskum, G., additional, Fernandez-Alfonso, M., additional, Guzman-Ruiz, R., additional, Somoza, B., additional, Gil-Ortega, M., additional, Attane, C., additional, Castan-Laurell, I., additional, Valet, P., additional, Ruiz-Gayo, M., additional, Denissevich, T., additional, Schrepper, A., additional, Schwarzer, M., additional, Amorim, P., additional, Schoepe, M., additional, Mohr, F., additional, Doenst, T., additional, Chiellini, G., additional, Ghelardoni, S., additional, Saba, A., additional, Marchini, M., additional, Frascarelli, S., additional, Raffaelli, A., additional, Scanlan, T., additional, Zucchi, R., additional, Van Den Akker, N., additional, Molin, D., additional, Kolk, F., additional, Jeukens, F., additional, Olde Engberink, R., additional, Post, M., additional, Verbruggen, S., additional, Schulten, H., additional, Rochais, F., additional, Kelly, R., additional, Aberg, M., additional, Johnell, M., additional, Wickstrom, M., additional, Siegbahn, A., additional, Dimitrakis, P., additional, Groppalli, V., additional, Ott, D., additional, Seifriz, F., additional, Suter, T., additional, Zuppinger, C., additional, Kashcheyeu, Y., additional, Mueller, R., additional, Wiesen, M., additional, Gruendemann, D., additional, Falcao-Pires, I., additional, Fontes-Sousa, A., additional, Lopes-Conceicao, L., additional, Bras-Silva, C., additional, Leite-Moreira, A., additional, Bukauskas, F., additional, Palacios-Prado, N., additional, Norheim, F., additional, Raastad, T., additional, Thiede, B., additional, Drevon, C., additional, Haugen, F., additional, Lindner, D., additional, Westermann, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschoepe, C., additional, Horn, M., additional, Graham, H., additional, Hall, M., additional, Richards, M., additional, Clarke, J., additional, Dibb, K., additional, Trafford, A., additional, Cheng, C.-F., additional, Lin, H., additional, Eigeldiger-Berthou, S., additional, Buntschu, P., additional, Frobert, A., additional, Flueck, M., additional, Tevaearai, H., additional, Kadner, A., additional, Mikhailov, A., additional, Torrado, M., additional, Centeno, A., additional, Lopez, E., additional, Lourido, L., additional, Castro Beiras, A., additional, Popov, T., additional, Srdanovic, I., additional, Petrovic, M., additional, Canji, T., additional, Kovacevic, M., additional, Jovelic, A., additional, Sladojevic, M., additional, Panic, G., additional, Kararigas, G., additional, Fliegner, D., additional, Regitz-Zagrosek, V., additional, De La Rosa Sanchez, A., additional, Dominguez, J., additional, Sedmera, D., additional, Franco, D., additional, Medunjanin, S., additional, Burgbacher, F., additional, Han, W., additional, Zhang, J., additional, Gao, X., additional, Bayliss, C., additional, Song, W., additional, Stuckey, D., additional, 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additional, D'amati, G., additional, Nediani, C., additional, Raimondi, L., additional, Micova, P., additional, Balkova, P., additional, Kolar, F., additional, Neckar, J., additional, Novak, F., additional, Novakova, O., additional, Schuchardt, M., additional, Pruefer, N., additional, Pruefer, J., additional, Jankowski, V., additional, Jankowski, J., additional, Su, Y., additional, Zervou, S., additional, Seidel, B., additional, Radovits, T., additional, Barnucz, E., additional, Aggeli, I., additional, Kefaloyianni, E., additional, Beis, I., additional, Gaitanaki, C., additional, Lacerda, L., additional, Somers, S., additional, Paur, H., additional, Nikolaev, V., additional, Lyon, A., additional, Silva, S., additional, Gomes, M., additional, Ferreira, P., additional, Capuano, V., additional, Ferron, L., additional, Ruchon, Y., additional, Ben Mohamed, F., additional, Renaud, J.-F., additional, Goncalves, N., additional, Gavina, C., additional, Pinho, S., additional, Moura, C., additional, Amorim, M., additional, Pinho, P., additional, Christ, T., additional, Molenaar, P., additional, Kaumann, A., additional, Kletsiou, E., additional, Giannakopoulou, M., additional, Bozas, E., additional, Iliodromitis, E., additional, Anastasiou-Nana, M., additional, Papathanassoglou, E., additional, Chottova Dvorakova, M., additional, Mistrova, E., additional, Slavikova, J., additional, Hynie, S., additional, Sida, P., additional, Klenerova, V., additional, Zakrzewicz, A., additional, Hoffmann, C., additional, Hohberg, M., additional, Chlench, S., additional, Maroski, J., additional, Drab, M., additional, Siegel, G., additional, Pries, A., additional, Schrot, G., additional, Wilck, N., additional, Fechner, M., additional, Arias, A., additional, Meiners, S., additional, Baumann, G., additional, Stangl, V., additional, Stangl, K., additional, Ludwig, A., additional, Christ, A., additional, Eijgelaar, W., additional, Daemen, M., additional, Penfold, M., additional, Schall, T., additional, Hintenberger, R., additional, Kaun, C., additional, Pfaffenberger, S., additional, Maurer, G., additional, Huber, K., additional, Wojta, J., additional, Demyanets, S., additional, Titov, V., additional, Chin-Dusting, J., additional, Vaisman, B., additional, Khong, S., additional, Remaley, A., additional, Andrews, K., additional, Hoeper, A., additional, Khalid, A., additional, Fuglested, B., additional, Aasum, E., additional, Larsen, T., additional, Diebold, I., additional, Petry, A., additional, Djordjevic, T., additional, Belaiba, R., additional, Fratz, S., additional, Hess, J., additional, Kietzmann, T., additional, Goerlach, A., additional, Chess, D., additional, Walsh, K., additional, Van Der Velden, J., additional, Moreira-Goncalves, D., additional, Paulus, W., additional, Niessen, H., additional, Perlini, S., additional, Azibani, F., additional, Tournoux, F., additional, Fazal, L., additional, Polidano, E., additional, Merval, R., additional, Chatziantoniou, C., additional, Samuel, J., additional, Delcayre, C., additional, Mgandela, P., additional, Brooksbank, R., additional, Maswanganyi, T., additional, Woodiwiss, A., additional, Norton, G., additional, Makaula, S., additional, Bucciantini, M., additional, Spinelli, V., additional, Coppini, R., additional, Russo, E., additional, Stefani, M., additional, Sukumaran, V., additional, Watanabe, K., additional, Ma, M., additional, Thandavarayan, R., additional, Azrozal, W., additional, Sari, F., additional, Shimazaki, H., additional, Kobayashi, Y., additional, Roleder, T., additional, Golba, K., additional, Deja, M., additional, Malinowski, M., additional, Wos, S., additional, Grebe, M., additional, Preissner, K., additional, Ercan, E., additional, Guven, A., additional, Asgun, F., additional, Ickin, M., additional, Ercan, F., additional, Kaplan, A., additional, Yavuz, O., additional, Bagla, S., additional, Kuka, J., additional, Vilskersts, R., additional, Vavers, E., additional, Liepins, E., additional, Dambrova, M., additional, Duerr, G., additional, Suchan, G., additional, Heuft, T., additional, Klaas, T., additional, Zimmer, A., additional, Welz, A., additional, Fleischmann, B., additional, Dewald, O., additional, Voelkl, J., additional, Haubner, B., additional, Kremser, C., additional, Mayr, A., additional, Klug, G., additional, Reiner, M., additional, Pachinger, O., additional, Metzler, B., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Pelogeykina, Y., additional, Khatri, D., additional, Studneva, I., additional, Bencsik, P., additional, Kocsis, G., additional, Shamloo, M., additional, Woodburn, K., additional, Szucs, G., additional, Kupai, K., additional, Csont, C., additional, Kocsisne Fodor, G., additional, Monostori, P., additional, and Turi, S., additional

Published
2010
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35. The role of Na+/H+ exchange in ischemia-reperfusion

Author

Piper, H. M., Balser, C., Ladilov, Y. V., Schäfer, M., Siegmund, B., Ruiz-Meana, M., and Garcia-Dorado, D.

Abstract

In ischemia the cytosol of cardiomyocytes acidifies; this is reversed upon reperfusion. One of the major pHi-regulating transport systems involved is the Na+/H+ exchanger. Inhibitors of the Na+/H+ exchanger have been found to more effectively protect ischemic-reperfused myocardium when administered before and during ischemia than during reperfusion alone. It has been hypothesized that the protection provided by pre-ischemic administration is due to a reduction in Na+ and secondary Ca2+ influx. Under reperfusion conditions Na+/H+ exchange inhibition also seems protective since it prolongs intracellular acidosis which can prevent hypercontracture. In detail, however, the mechanisms by which Na+/H+ exchange inhibition provides protection in ischemic-reperfused myocardium are still not fully identified.

Published
1996
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36. Sodium/Hydrogen Exchanger Inhibition Reduces Myocardial Reperfusion Edema After Normothermic Cardioplegia

Author

Tritto, F.P., Inserte, J., Garcia-Dorado, D., Ruiz-Meana, M., and Soler-Soler, J.

Abstract

Objective: The hypothesis was that Na^+/H^+ exchange occurring during normothermic cardioplegia contributes to the development of myocardial edema during subsequent reperfusion and impairs functional recovery. Methods: Rat hearts were perfused in a Langendorff apparatus and submitted to 60 minutes of normothermic cardioplegia and 90 minutes of reperfusion. Hearts were allocated to one of four groups (n = 8): inhibition of Na^+/H^+ exchanger with HOE642 throughout the whole experiment (HOE group), only during cardioplegia (HOE-C) or during reperfusion (HOE-R), and a control group. Results: In HOE and HOE-C groups, myocardial water content at the end of reperfusion was lower than in the HOE-R and control groups (526 +/- 19 and 533 +/- 18 ml/100 gm dry tissue vs 632 +/- 25 and 634 +/- 17 ml/100 gm dry tissue, respectively, p = 0.001), left ventricular end-diastolic pressure increased less after reperfusion (46.6 +/- 9.7 and 63.2 +/- 10.0 mm Hg vs 75.1 +/- 4.3 mm Hg and 85.7 +/- 8.9 mm Hg, respectively, p = 0.006), and recovery of left ventricular developed pressure was better (46.7% and 45.8% vs 4.5% and 9.8%, p = 0.048). Relative to the control group, total lactate dehydrogenase release during reperfusion was reduced by 80.2%, 69.3% and 36% in HOE, HOE-C, and HOE-R groups, respectively. Conclusion: Inhibition of the Na^+/H^+ exchange during normothermic cardioplegia reduces myocardial edema and necrosis during subsequent reperfusion, improving functional recovery. Inhibition of Na^+/H^+ exchange during reperfusion only has a much smaller effect. (J Thorac Cardiovasc Surg 1998;115:709-15)

Published
1998
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37. The (still) unknown mechanism of ischemic preconditioning: possible involvement of reduced Na+/H+ exchange.

Author

Garcia-Dorado, D. and Ruiz-Meana, M.

Abstract

These observations support the view that the mechanism responsible for the anti-infarct effect of ischemic preconditioning is far from being completely understood. The potential involvement of reduced Na+/H+ exchange in this effect cannot be ruled out on the basis of currently available, information and illustrates the uncompletness of our knowledge of the molecular mechanisms responsible for the cardioprotective effect of preconditioning. The potential role of attenuated Na+/H+ exchange in this effect cannot be easily integrated into the signal cascade of messengers proposed for preconditioning, but may be seen as a mechanism acting in parallel. The importance of this mechanism may depend on the conditions, as initial glycogen content or alternative routes of Na+ gain. These conditions may be different in the isolated crystalline perfused heart as compared to in situ myocardium. Further studies are necessary to resolve the possible role of attenuated acidosis and Na+/H+ exchange in ischemic preconditioning. These studies should aim to dissociate glycogen depletion, attenuated acidosis, and reduced Na+/H+ exchange in situ preconditioned myocardium. [ABSTRACT FROM AUTHOR]

Published
1997
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41. P441 Defective SR-mitochondria interaction and Ca2+ transfer in aged mouse cardiomyocytes.

Author

Fernandez-Sanz, C, Ruiz-Meana, M, Miro-Casas, E, Castellano, J, Barba, I, Nunez, E, Vazquez, J, and Garcia-Dorado, D

Subjects
*SARCOPLASMIC reticulum, *MITOCHONDRIA, *HEART cells, *DISEASE susceptibility, *ARTIFICIAL respiration, *LABORATORY mice
Abstract

Mitochondrial alterations are critically involved in the increased susceptibility to disease of the aging heart. We investigated the role of sarcoplasmic reticulum (SR)-mitochondria communication in myocardial calcium handling during aging.Methods and results: In subsarcolemmal and interfibrillar mitochondria isolated from old (>20 months) and young (<6 months) mouse hearts no differences in resting respiration through the different complexes were detected, but maximal ADP-stimulated O2 consumption was reduced in aged interfibrillar mitochondria. Accordingly, resting mitochondrial membrane potential in cardiomyocytes and ATP/phosphocreatine in intact myocardium (NMR spectroscopy) were preserved in old mice. Second generation proteomics disclosed an increase in mitochondrial protein oxidation during aging. Since mitochondrial Ca2+ regulates both energy production and oxidative status, we investigated whether aging affects mitochondrial Ca2+ uptake. No age-dependent differences were found in Ca2+ uptake kinetics in isolated mitochondria. By contrast, mitochondrial Ca2+ uptake resulting from SR transfer was significantly reduced in old cardiomyocytes, despite no changes in SR Ca2+ content. Immunocolocalization and proximity ligation assay identified defective communication between mitochondrial VDAC and SR ryanodine receptor (RyR) during aging, with adverse functional consequences on SR (Ca2+ transients and sparks). Age-dependent alterations in SR Ca2+ transfer to mitochondria could be reproduced in young cardiomyoctes after pharmacological disruption of the connection between both organelles, an intervention that had no effect in old cardiomyocytes or isolated mitochondria.Conclusion: Defective SR-mitochondria communication underlies inefficient Ca2+ exchange between both organelles that could be responsible, at least in part, for inadequate energy demand/supply matching in the aging heart. [ABSTRACT FROM PUBLISHER]

Published
2014
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42. P166 Extracellular RNA in cardiac ischemia/reperfusion injury: prevention of heart failure and cell damage by RNase1.

Author

Cabrera-Fuentes, H A, Ruiz-Meana, M, Kostin, S, Lecour, S, Hausenloy, DJ, Garcia-Dorado, DJ, Schluter, KD, and Preissner, KT

Subjects
*RNA, *REPERFUSION injury, *HEART failure, *RIBONUCLEASES, *MORTALITY, *MYOCARDIAL infarction
Abstract

Despite optimal therapy, the morbidity and mortality of patients presenting with an acute myocardial infarction (MI) remain significant. Extracellular RNA (eRNA), exposed after cell damage, serves as cofactor for coagulation proteases and cytokines thereby promoting their procoagulant and proinflammatory functions in vivo. Following myocardial ischemia/reperfusion (I/R) in mice or I/R induced in the isolated Langendorff heart, increased eRNA levels were found together with cell injury markers. Likewise, eRNA was released from cardiomyocytes under hypoxia and subsequently induced tumor-necrosis-factor-a (TNF-α) liberation by activation of TNF-α converting enzyme (TACE) and provoked cardiomyocyte death. Conversely, TNF-a promoted eRNA release especially under hypoxia, feeding a vicious cell damaging cycle during I/R. Administration of RNase1 or TAPI (TACE-inhibitor) prevented cell death and myocardial infarction. Likewise, RNase1 significantly reduced I/R-mediated energy exhaustion, opening of mitochondrial permeability transition pores (mPTP) as well as oxidative damage in cardiomyocytes. Together, RNase1 as well as inhibition of TACE provide novel therapeutic regimen to interfere with the adverse eRNA-TNF-a interplay and significantly reduce or prevent the pathological outcome of ischemic heart injury. [ABSTRACT FROM PUBLISHER]

Published
2014
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43. P375 Ischemic postconditioning delays recovery of passive myocardial electrical properties independently of connexin 43 expression.

Author

Rodriguez-Sinovas, A, Diez, E, Sanchez, JA, Ruiz-Meana, M, and Garcia-Dorado, D

Subjects
CORONARY disease, MYOCARDIAL infarction risk factors, ELECTRIC properties of hearts, CONNEXINS, GENE expression, MYOCARDIAL revascularization
Abstract

Background: Ventricular arrhythmias are a common clinical manifestation in patients with acute myocardial infarction submitted to coronary revascularizaton. Reperfusion arrhythmias have been associated with successful myocardial reperfusion during thrombolytic therapy, but they have been also suggested to be a marker of large infarct size and worse prognosis. Ischemic postconditioning (PostC) has been shown to reduce the incidence of reperfusion arrhythmias. However, the mechanisms involved in the antiarrhythmic effects of ischemic PostC are not well known. The aims of this study were (1) to analyze the electrophysiologycal effects of ischemic PostC on passive myocardial electrical properties, as a surrogate of gap junctional communication, in isolated rat hearts, and (2) to assess the involvement of connexin 43 (Cx43) in these effects, using isolated hearts from wild-type mice and from mice devoid of connexin 43.Methods and results: Isolated rat hearts were submitted to 20 min of global ischemia followed by 25 min of reperfusion. Myocardial electrical impedance (tissue resistivity and phase angle) was assessed using a four-electrode probe, placed in the left ventricular free wall, at 7 kHz. Global ischemia induced a marked rise in resistivity and a decrease in phase angle (p≤0.05). Ischemic PostC (6 cycles of 10 seconds of reperfusion/ischemia, n=7), applied at the onset of reperfusion, slowed and delayed, by about 4 min, recovery of tissue resistivity as compared with recovery in control hearts. To analyze the involvement of Cx43 in these changes, isolated hearts from two Cx43-defficient mice (Cx43KI32 mice, in which the coding region for Cx43 is replaced by that of Cx32, and a inducible knock-out model, in which a marked reduction in Cx43 expression is achieved after 4-hydroxytamoxifen administration) were submitted to 30 min of global ischemia followed by reperfusion. Hearts from wild-type animals and from both homozygous Cx43KI32 mice (n=6-8) and Cx43Cre-ER(T)/fl mice (n=7-8), were protected against infarction by ischemic PostC (6 cycles of 10 seconds of reperfusion/ischemia). Similar to findings in isolated rat and mice wild-type hearts, ischemic PostC still delayed recovery of tissue resisitvity (about 3 min) in hearts from Cx43-defficient animals.Conclusions: Ischemic PostC delays recovery of tissue resistivity during reperfusion, but this effect is indepenent of Cx43 expression.. The mechanisms of the antiarrhythmic effect of ischemic postconditioning remain elusive. [ABSTRACT FROM AUTHOR]

Published
2014
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44. P141 Prevention of microtubule disruption with paclitaxel does not protect against infarction in isolated rat hearts.

Author

Rodriguez-Sinovas, A, Abad, E, Sanchez, JA, Fernandez-Sanz, C, Inserte, J, Ruiz-Meana, M, and Garcia-Dorado, D

Subjects
MICROTUBULES, PACLITAXEL, MYOCARDIAL infarction, EUKARYOTES, CYTOSKELETON, LABORATORY rats
Abstract

Background: Microtubules are highly dynamic polymers present in eukaryote cells that are essential components of cell cytoskeleton. They play an important role in intracellular transport, in maintaining organelle organization and function, and in transmitting mechanical forces within the myocardium. However, this intracellular network becomes disrupted during myocardial ischemia/reperfusion, and it has been proposed that microtubule disruption is an early sign of irreversible ischemic injury, and that prevention of microtubule disruption during ischemia-reperfusion could be beneficial. In this study we aimed to assess the effects of prevention of microtubule disruption with paclitaxel on ischemia/reperfusion injury in both isolated rat cardiomyocytes and isolated, Langendorff-perfused, rat hearts.Methods and results: Isolated rat cardiomyocytes were submitted to normoxia (1h), or to 50 min of anoxia (pH 6.4, 0% O2, 37° C) and 15 min reoxygenation, without or with treatment during anoxia with the microtubule stabilizer paclitaxel (10 μM) or the inhibitor of microtubule polymerization colchicine (5 μM). The condition of microtubule network was assessed by immunofluorescence detection of α-tubulin. Anoxia/reoxygenation leads to disruption of the microtubule network before the onset of ischemic contracture (650±21 vs. 328±11 arbitrary units of fluorescence (auf), p≤0.05). Paclitaxel attenuated both microtubule disruption (377±15 auf, p≤0.05 vs. anoxia/reoxygenation) and the incidence of hypercontracture (31±7 % vs. 56±8 % in anoxia/reoxygenation, p≤0.05) induced by anoxia/reoxygenation, whereas treatment with colchicine mimicked the effects of anoxia/reoxygenation (fluorescence: 188±16 auf, p≤0.01 vs. anoxia/reoxygenation; hypercontracture: 65±7 %). In isolated rat hearts under normoxic conditions, paclitaxel induced a concentration-dependent increase in perfusion pressure and a decrease in heart rate and left ventricular developed pressure. Despite protection against cell hypercontracture, paclitaxel pretreatment did not modify infarct size (60.37±2.27 % in control hearts vs. 58.75±10.25, 55.44±10.32 and 50.06±10.14 % in hearts pretreated with 10-6, 3 10-6 and 10-5 M, of paclitaxel respectively), LDH release or functional recovery after 60 min of global ischemia and reperfusion in isolated rat hearts.Conclusions: Microtubule stabilization with paclitaxel reduces hypercontracture in isolated rat cardiomyocytes but does not protect against infarction in isolated rat hearts. [ABSTRACT FROM AUTHOR]

Published
2014
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45. Spontaneous reperfusion enhances succinate concentration in peripheral blood from stemi patients but its levels does not correlate with myocardial infarct size or area at risk

Author

Marta Consegal, Ignasi Barba, Bruno García del Blanco, Imanol Otaegui, José F. Rodríguez-Palomares, Gerard Martí, Bernat Serra, Neus Bellera, Manuel Ojeda-Ramos, Filipa Valente, Maria Ángeles Carmona, Elisabet Miró-Casas, Antonia Sambola, Rosa María Lidón, Jordi Bañeras, José Antonio Barrabés, Cristina Rodríguez, Begoña Benito, Marisol Ruiz-Meana, Javier Inserte, Ignacio Ferreira-González, Antonio Rodríguez-Sinovas, Institut Català de la Salut, [Consegal M, Benito B, Ruiz-Meana M, Inserte J, Rodríguez-Sinovas A] Grup de Recerca de Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Servei de Cardiologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, Madrid, Spain. [Barba I] Grup de Recerca de Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Servei de Cardiologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, Madrid, Spain. Faculty of Medicine, University of Vic - Central University of Catalonia (UVicUCC), Vic, Spain. [García Del Blanco B, Otaegui I, Rodríguez-Palomares JF, Martí G, Serra B, Bellera N, Ojeda-Ramos M, Valente F, Carmona MÁ, Miró-Casas E, Sambola A, Lidón RM, Bañeras J, Barrabés JA] Grup de Recerca de Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Servei de Cardiologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, Madrid, Spain. [Ferreira-González I] Grup de Recerca de Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Servei de Cardiologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Epidemiología y Salud Pública, CIBERESP, Instituto de Salud Carlos III, Madrid, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
Surgical Procedures, Operative::Cardiovascular Surgical Procedures::Reperfusion [ANALYTICAL, DIAGNOSTIC AND THERAPEUTIC TECHNIQUES, AND EQUIPMENT], Infart de miocardi, Multidisciplinary, Reperfusió (Fisiologia), compuestos orgánicos::ácidos carboxílicos::ácidos acíclicos::ácidos dicarboxílicos::succinatos::ácido succínico [COMPUESTOS QUÍMICOS Y DROGAS], Organic Chemicals::Carboxylic Acids::Acids, Acyclic::Dicarboxylic Acids::Succinates::Succinic Acid [CHEMICALS AND DRUGS], intervenciones quirúrgicas::procedimientos quirúrgicos cardiovasculares::reperfusión [TÉCNICAS Y EQUIPOS ANALÍTICOS, DIAGNÓSTICOS Y TERAPÉUTICOS], enfermedades cardiovasculares::enfermedades cardíacas::isquemia miocárdica::infarto de miocardio [ENFERMEDADES], Cardiovascular Diseases::Heart Diseases::Myocardial Ischemia::Myocardial Infarction [DISEASES]
Abstract

Cardiovascular biology; Diagnostic markers; Prognostic markers Biología cardiovascular; Marcadores de diagnóstico; Marcadores pronósticos Biologia cardiovascular; Marcadors diagnòstics; Marcadors pronòstics Succinate is enhanced during initial reperfusion in blood from the coronary sinus in ST-segment elevation myocardial infarction (STEMI) patients and in pigs submitted to transient coronary occlusion. Succinate levels might have a prognostic value, as they may correlate with edema volume or myocardial infarct size. However, blood from the coronary sinus is not routinely obtained in the CathLab. As succinate might be also increased in peripheral blood, we aimed to investigate whether peripheral plasma concentrations of succinate and other metabolites obtained during coronary revascularization correlate with edema volume or infarct size in STEMI patients. Plasma samples were obtained from peripheral blood within the first 10 min of revascularization in 102 STEMI patients included in the COMBAT-MI trial (initial TIMI 1) and from 9 additional patients with restituted coronary blood flow (TIMI 2). Metabolite concentrations were analyzed by 1H-NMR. Succinate concentration averaged 0.069 ± 0.0073 mmol/L in patients with TIMI flow ≤ 1 and was significantly increased in those with TIMI 2 at admission (0.141 ± 0.058 mmol/L, p

Published
2023

46. Connexin 43 in Mitochondria: What Do We Really Know About Its Function?

Author

Kerstin Boengler, Luc Leybaert, Marisol Ruiz-Meana, Rainer Schulz, Institut Català de la Salut, [Boengler K, Schulz R] Institute of Physiology, Justus-Liebig University, Giessen, Germany. [Leybaert L] Department of Basic and Applied Medical Sciences—Physiology Group, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium. [Ruiz-Meana M] Grup de Recerca en Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
Cor - Fisiologia patològica, connexin, Other subheadings::Other subheadings::/physiopathology [Other subheadings], Otros calificadores::Otros calificadores::/fisiopatología [Otros calificadores], hemichannel, Physiology, ischemia-reperfusion injury, Connexines - Metabolisme, Biology and Life Sciences, Amino Acids, Peptides, and Proteins::Proteins::Membrane Proteins::Membrane Transport Proteins::Connexins::Connexin 43 [CHEMICALS AND DRUGS], Other subheadings::Other subheadings::/metabolism [Other subheadings], enfermedades cardiovasculares::enfermedades cardíacas [ENFERMEDADES], mitochondria, Cardiovascular Diseases::Heart Diseases [DISEASES], preconditioning, Physiology (medical), aminoácidos, péptidos y proteínas::proteínas::proteínas de membranas::proteínas de transporte de membrana::conexinas::conexina 43 [COMPUESTOS QUÍMICOS Y DROGAS], Medicine and Health Sciences, GJA1-20k, Cor - Malalties, Otros calificadores::Otros calificadores::/metabolismo [Otros calificadores]
Abstract

Connexin: Ischemia-reperfusion injury; Mitochondria Conexina; Lesión por isquemia-reperfusión; Mitocondrias Connexina; Lesió per isquèmia-reperfusió; Mitocondris Connexins are known for their ability to mediate cell-cell communication via gap junctions and also form hemichannels that pass ions and molecules over the plasma membrane when open. Connexins have also been detected within mitochondria, with mitochondrial connexin 43 (Cx43) being the best studied to date. In this review, we discuss evidence for Cx43 presence in mitochondria of cell lines, primary cells and organs and summarize data on its localization, import and phosphorylation status. We further highlight the influence of Cx43 on mitochondrial function in terms of respiration, opening of the mitochondrial permeability transition pore and formation of reactive oxygen species, and also address the presence of a truncated form of Cx43 termed Gja1-20k. Finally, the role of mitochondrial Cx43 in pathological conditions, particularly in the heart, is discussed. KB is funded by the German Research Foundation (BO 2955/4-1). LL is supported by the Research Foundation Flanders (FWO) grant numbers G.0527.18N and G040720N. MR-M is supported by the Instituto de Salud Carlos III of the Spanish Ministry of Health (FIS-PI19-01196) and a grant from the Sociedad Española de Cardiología (SEC/FEC-INV- BAS 217003).

Published
2022
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47. Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy

Author

David Aluja, Sara Delgado-Tomás, Marisol Ruiz-Meana, José A. Barrabés, Javier Inserte, Institut Català de la Salut, [Aluja D, Delgado-Tomás S] Grup de Recerca en Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Ruiz-Meana M, Barrabés JA, Inserte J] Grup de Recerca en Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. Centro de Investigación en Red de Enfermedades Cardiovasculares (CIBERCV), 28029 Madrid, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
Heart Failure, Cardiovascular Diseases::Heart Diseases::Heart Failure [DISEASES], Calpain, Organic Chemistry, Calcium-Binding Proteins, Enzims - Ús terapèutic, Otros calificadores::Otros calificadores::/farmacoterapia [Otros calificadores], Cardiomegaly, General Medicine, Other subheadings::Other subheadings::/drug therapy [Other subheadings], enfermedades cardiovasculares::enfermedades cardíacas::insuficiencia cardíaca [ENFERMEDADES], Catalysis, Computer Science Applications, Inorganic Chemistry, Enzymes and Coenzymes::Enzymes::Hydrolases::Peptide Hydrolases::Cysteine Proteases::Cysteine Endopeptidases::Calpain [CHEMICALS AND DRUGS], enzimas y coenzimas::enzimas::hidrolasas::péptido hidrolasas::cisteína proteasas::cisteína endopeptidasas::calpaína [COMPUESTOS QUÍMICOS Y DROGAS], Animals, Physical and Theoretical Chemistry, Insuficiència renal aguda - Tractament, Molecular Biology, Spectroscopy
Abstract

Calpain; Calpastatin; Myocardial hypertrophy Calpaína; Calpastatina; Hipertrofia miocárdica Calpaïna; Calpastatina; Hipertròfia miocàrdica Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, represents an independent risk factor for the development of heart failure, and its prevention constitutes a clinical objective. Recent studies performed in preclinical animal models support the contribution of the Ca2+-dependent cysteine proteases calpains in regulating the hypertrophic process and highlight the feasibility of their long-term inhibition as a pharmacological strategy. In this review, we discuss the existing evidence implicating calpains in the development of cardiac hypertrophy, as well as the latest advances in unraveling the underlying mechanisms. Finally, we provide an updated overview of calpain inhibitors that have been explored in preclinical models of cardiac hypertrophy and the progress made in developing new compounds that may serve for testing the efficacy of calpain inhibition in the treatment of pathological cardiac hypertrophy. This study was funded by the Instituto de Salud Carlos III of the Spanish Ministry of Health FIS-PI20/01681) and the research network CIBERCV (CB16/11/00479).

Published
2022

48. Defective dimerization of FoF1‐ATP synthase secondary to glycation favors mitochondrial energy deficiency in cardiomyocytes during aging

Author

Diana Bou‐Teen, Celia Fernandez‐Sanz, Elisabet Miro‐Casas, Zuzana Nichtova, Elena Bonzon‐Kulichenko, Kelly Casós, Javier Inserte, Antonio Rodriguez‐Sinovas, Begoña Benito, Shey‐Shing Sheu, Jesús Vázquez, Ignacio Ferreira‐González, Marisol Ruiz‐Meana, Instituto de Salud Carlos III, Ministerio de Salud (España), Sociedad Española de Cardiología, Institut Català de la Salut, [Bou-Teen D, Miro-Casas E, Casós K, Inserte J, Rodriguez-Sinovas A, Benito B, Ruiz-Meana M] Grup de Recerca en Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Fernandez-Sanz C, Sheu SS] Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, USA. [Nichtova Z] MitoCare Center for Mitochondrial Imaging Research and Diagnostics, Department of Pathology, Anatomy & Cell Biol., Thomas Jefferson University, Philadelphia, USA. [Bonzon-Kulichenko E, Vázquez J] Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain. Cardiovascular Proteomics Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain. [Ferreira-González I] Grup de Recerca en Malalties Cardiovasculars, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
Glycation End Products, Advanced, Aging, Mitochondrial Permeability Transition Pore, Other subheadings::Other subheadings::/metabolism [Other subheadings], Cell Biology, Mitochondrial Proton-Translocating ATPases, Mitochondria, Heart, Mice, Adenosine Triphosphate, Animals, Myocytes, Cardiac, Calcium, Mitocondris - Malalties, Cèl·lules - Envelliment, células::estructuras celulares::espacio intracelular::citoplasma::estructuras citoplasmáticas::orgánulos::mitocondrias::mitocondrias musculares::mitocondrias cardíacas [ANATOMÍA], Dimerization, Cells::Cellular Structures::Intracellular Space::Cytoplasm::Cytoplasmic Structures::Organelles::Mitochondria::Mitochondria, Muscle::Mitochondria, Heart [ANATOMY], Otros calificadores::Otros calificadores::/metabolismo [Otros calificadores]
Abstract

Aging; Dicarbonyl stress; Mitochondria Envelliment; Estrès dicarbonílic; Mitocondris Envejecimiento; Estrés dicarbonílico; Mitocondrias Aged cardiomyocytes develop a mismatch between energy demand and supply, the severity of which determines the onset of heart failure, and become prone to undergo cell death. The FoF1-ATP synthase is the molecular machine that provides >90% of the ATP consumed by healthy cardiomyocytes and is proposed to form the mitochondrial permeability transition pore (mPTP), an energy-dissipating channel involved in cell death. We investigated whether aging alters FoF1-ATP synthase self-assembly, a fundamental biological process involved in mitochondrial cristae morphology and energy efficiency, and the functional consequences this may have. Purified heart mitochondria and cardiomyocytes from aging mice displayed an impaired dimerization of FoF1-ATP synthase (blue native and proximity ligation assay), associated with abnormal mitochondrial cristae tip curvature (TEM). Defective dimerization did not modify the in vitro hydrolase activity of FoF1-ATP synthase but reduced the efficiency of oxidative phosphorylation in intact mitochondria (in which membrane architecture plays a fundamental role) and increased cardiomyocytes’ susceptibility to undergo energy collapse by mPTP. High throughput proteomics and fluorescence immunolabeling identified glycation of 5 subunits of FoF1-ATP synthase as the causative mechanism of the altered dimerization. In vitro induction of FoF1-ATP synthase glycation in H9c2 myoblasts recapitulated the age-related defective FoF1-ATP synthase assembly, reduced the relative contribution of oxidative phosphorylation to cell energy metabolism, and increased mPTP susceptibility. These results identify altered dimerization of FoF1-ATP synthase secondary to enzyme glycation as a novel pathophysiological mechanism involved in mitochondrial cristae remodeling, energy deficiency, and increased vulnerability of cardiomyocytes to undergo mitochondrial failure during aging. This work was supported by the Instituto de Salud Carlos III of the Spanish Ministry of Health (FIS-PI19-01196) and a grant from the Sociedad Española de Cardiología (SEC/FEC-INV-BAS 217003)

Published
2022

49. Cardiac-Specific Overexpression of ERRγ in Mice Induces Severe Heart Dysfunction and Early Lethality

Author

Marc Velilla, Jaime Lasheras, Rafael Simó, Monica Zamora, Marcos Poncelas, Rosario Pardo, Josep A. Villena, Núria Salvatella, Marisol Ruiz-Meana, Institut Català de la Salut, [Lasheras J, Pardo R, Velilla M, Salvatella N] Laboratori de Metabolisme i Obesitat, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. [Poncelas M, Ruiz-Meana M] Laboratori de Cardiologia Experimental, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. [Simó R] Unitat de Diabetis i Metabolisme, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. CIBER on Diabetes and Associated Metabolic Diseases (CIBERDEM), 28029 Madrid, Spain. [Villena JA] Laboratori de Metabolisme i Obesitat, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. CIBER on Diabetes and Associated Metabolic Diseases (CIBERDEM), 28029 Madrid, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
0301 basic medicine, Cardiovascular Diseases::Heart Diseases::Cardiomegaly::Cardiomyopathy, Dilated [DISEASES], 030204 cardiovascular system & hematology, células::células musculares::miocitos cardíacos [ANATOMÍA], Mice, 0302 clinical medicine, Fibrosis, Diabetic cardiomyopathy, Medicine, Myocytes, Cardiac, Biology (General), Receptor, Spectroscopy, Otros calificadores::Otros calificadores::/metabolismo [Otros calificadores], cardiac dysfunction, Dilated cardiomyopathy, Other subheadings::Other subheadings::/metabolism [Other subheadings], General Medicine, Computer Science Applications, Cell biology, Chemistry, Receptors, Estrogen, estrogen-related receptors, Cardiac function curve, Cardiomyopathy, Dilated, Programmed cell death, QH301-705.5, enfermedades cardiovasculares::enfermedades cardíacas::cardiomegalia::miocardiopatía dilatada [ENFERMEDADES], Cells::Muscle Cells::Myocytes, Cardiac [ANATOMY], Mice, Transgenic, transgenic mice, Catalysis, Article, Inorganic Chemistry, 03 medical and health sciences, Animals, Physical and Theoretical Chemistry, QD1-999, Molecular Biology, business.industry, Myocardium, Organic Chemistry, medicine.disease, Miocardi - Malalties - Metabolisme, Cor - Metabolisme, Mice, Inbred C57BL, 030104 developmental biology, Nuclear receptor, Heart failure, business
Abstract

Disfunció cardíaca; Receptors relacionats amb estrògens; Ratolins transgènics Disfunción cardíaca; Receptores relacionados con el estrógeno; Ratones transgénicos Cardiac dysfunction; Estrogen-related receptors; Transgenic mice Proper cardiac function depends on the coordinated expression of multiple gene networks related to fuel utilization and mitochondrial ATP production, heart contraction, and ion transport. Key transcriptional regulators that regulate these gene networks have been identified. Among them, estrogen-related receptors (ERRs) have emerged as crucial modulators of cardiac function by regulating cellular metabolism and contraction machinery. Consistent with this role, lack of ERRα or ERRγ results in cardiac derangements that lead to functional maladaptation in response to increased workload. Interestingly, metabolic inflexibility associated with diabetic cardiomyopathy has been recently associated with increased mitochondrial fatty acid oxidation and expression of ERRγ, suggesting that sustained expression of this nuclear receptor could result in a cardiac pathogenic outcome. Here, we describe the generation of mice with cardiac-specific overexpression of ERRγ, which die at young ages due to heart failure. ERRγ transgenic mice show signs of dilated cardiomyopathy associated with cardiomyocyte hypertrophy, increased cell death, and fibrosis. Our results suggest that ERRγ could play a role in mediating cardiac pathogenic responses. Research was funded by “Fundació la Marató de TV3” (# 082610 to JAV) and by Instituto de Salud Carlos III (PI19/00167 to MZ, co-funded by European Regional Development Fund -FEDER- “A way to make Europe”).

Published
2021

50. Citric Acid Cycle Metabolites Predict Infarct Size in Pigs Submitted to Transient Coronary Artery Occlusion and Treated with Succinate Dehydrogenase Inhibitors or Remote Ischemic Perconditioning

Author

Begoña Benito, Marisol Ruiz-Meana, Javier Inserte, Norberto Núñez, Marta Consegal, Ignacio Ferreira-González, Antonio Rodríguez-Sinovas, Ignasi Barba, Institut Català de la Salut, [Consegal M, Benito B, Ruiz-Meana M, Inserte J, Rodríguez-Sinovas A] Grup de Recerca en Malalties Cardiovasculars, Servei de Cardiologia, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, 28029 Madrid, Spain. [Núñez N] Unitat d'Alta Tecnologia, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Barba I] Grup de Recerca en Malalties Cardiovasculars, Servei de Cardiologia, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, 28029 Madrid, Spain. Faculty of Medicine, University of Vic-Central University of Catalonia (UVicUCC), Can Baumann. Ctra. de Roda, 70, 08500 Vic, Spain. [Ferreira-González I] Grup de Recerca en Malalties Cardiovasculars, Servei de Cardiologia, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red (CIBER) de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, 28029 Madrid, Spain, and Vall d'Hebron Barcelona Hospital Campus

Subjects
0301 basic medicine, Swine, Endogeny, 030204 cardiovascular system & hematology, Pharmacology, ischemia-reperfusion, Cardiovascular Diseases::Heart Diseases::Myocardial Ischemia::Myocardial Infarction [DISEASES], chemistry.chemical_compound, 0302 clinical medicine, hemic and lymphatic diseases, Dicarboxylic Acids, Myocardial infarction, Biology (General), Enzyme Inhibitors, Ischemic Preconditioning, Spectroscopy, remote ischemic conditioning, biology, Àcid cítric - Metabolisme, Chemistry, Succinate dehydrogenase, Ischemia-reperfusion, metabolismo::metabolismo energético::metabolismo::ciclo del ácido cítrico [FENÓMENOS Y PROCESOS], Remote ischemic conditioning, Heart, General Medicine, enfermedades cardiovasculares::enfermedades cardíacas::isquemia miocárdica::infarto de miocardio [ENFERMEDADES], Computer Science Applications, Malonate, myocardial infarction, Other subheadings::Other subheadings::/administration & dosage [Other subheadings], sustancias macromoleculares::complejos multiproteicos::complejos multienzimáticos::succinato citocromo c oxidorreductasa::complejo II de transporte de electrones::succinato deshidrogenasa [COMPUESTOS QUÍMICOS Y DROGAS], QH301-705.5, Sodium, Citric Acid Cycle, chemistry.chemical_element, Catalysis, Great cardiac vein, Article, Inorganic Chemistry, 03 medical and health sciences, Metabolism::Energy Metabolism::Metabolism::Citric Acid Cycle [PHENOMENA AND PROCESSES], medicine, Animals, Physical and Theoretical Chemistry, Molecular Biology, QD1-999, Macromolecular Substances::Multiprotein Complexes::Multienzyme Complexes::Succinate Cytochrome c Oxidoreductase::Electron Transport Complex II::Succinate Dehydrogenase [CHEMICALS AND DRUGS], Otros calificadores::Otros calificadores::/administración & dosificación [Otros calificadores], Myocardium, Organic Chemistry, medicine.disease, succinate dehydrogenase, malonate, Citric acid cycle, Infart de miocardi, 030104 developmental biology, Coronary Occlusion, Inhibidors enzimàtics, Coronary occlusion, biology.protein, Biomarkers
Abstract

Succinate dehydrogenase (SDH) inhibition with malonate during reperfusion reduced myocardial infarction in animals, whereas its endogenous substrate, succinate, is detected in plasma from STEMI patients. We investigated whether protection by SDH inhibition is additive to that of remote ischemic perconditioning (RIC) in pigs submitted to transient coronary artery occlusion, and whether protective maneuvers influence plasma levels of citric acid cycle metabolites. Forty pigs were submitted to 40 min coronary occlusion and reperfusion, and allocated to four groups (controls, sodium malonate 10 mmol/L, RIC, and malonate + RIC). Plasma was obtained from femoral and great cardiac veins and analyzed by LC-MS/MS. Malonate, RIC, and malonate + RIC reduced infarct size (24.67 ± 5.98, 25.29 ± 3.92 and 29.83 ± 4.62% vs. 46.47 ± 4.49% in controls, p &lt, 0.05), but no additive effects were detected. Enhanced concentrations of succinate, fumarate, malate and citrate were observed in controls during initial reperfusion in the great cardiac vein, and most were reduced by cardioprotective maneuvers. Concentrations of succinate, fumarate, and malate significantly correlated with infarct size. In conclusion, despite the combination of SDH inhibition during reperfusion and RIC did not result in additive protection, plasma concentrations of selected citric acid cycle metabolites are attenuated by protective maneuvers, correlate with irreversible injury, and might become a prognosis tool in STEMI patients.

Published
2021

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