176 results on '"Ventura-Clapier R"'
Search Results
2. Sexual dimorphism of doxorubicin-mediated cardiotoxicity in adult rats: potential role of energy metabolism remodeling: 519
- Author
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Moulin, MMaryline, Piquereau, J, Mateo, P, Fortin, D, Gressette, M, Lefebvre, F, Ventura-Clapier, V, Garnier, A, and Ventura-Clapier, R
- Published
- 2014
3. Altered skeletal muscle mitochondrial biogenesis but improved endurance capacity in trained OPA1-deficient mice
- Author
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Caffin, F., Prola, A., Piquereau, J., Novotova, M., David, D. J., Garnier, A., Fortin, D., Alavi, M. V., Veksler, V., Ventura-Clapier, R., and Joubert, F.
- Published
- 2013
- Full Text
- View/download PDF
4. Potentiating exercise training with resveratrol
- Author
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Ventura-Clapier, R.
- Published
- 2012
- Full Text
- View/download PDF
5. P560Effects of estrogen and estrogen receptors on mitochondrial function in cardiac and skelatal muscle fibers
- Author
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Fliegner, D., Jost, J., Bugger, H., Ventura-Clapier, R., and Regitz-Zagrosek, V.
- Published
- 2012
6. Metabolism, Oxygen, Ischaemia and ProtectionP343Mitochondrial respiration is reduced after myocardial infarction in chronic ischemic myocardium as well as in the remote non-ischemic region
- Author
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Bito, V., Claus, P., Vermeulen, K., Huysmans, C., Ventura-Clapier, R., and Sipido, K.R.
- Published
- 2012
7. P6276Impact of the cardiac specific deletion of AMPKalpha2 on the contractile and metabolic phenotype of the heart in male and female mice
- Author
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Grimbert, L, primary, Sanz, M N, additional, Rucker-Martin, C, additional, Novotova, M, additional, Gressette, M, additional, Gomez, S, additional, Solgadi, A, additional, Dumont, F, additional, Ventura-Clapier, R, additional, Veksler, V, additional, Piquereau, J, additional, and Garnier, A, additional
- Published
- 2019
- Full Text
- View/download PDF
8. Metabolic and non-metabolic effects of cardiac-specific and inducible deletion of the AMPKalpha2 in female and male mice
- Author
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Grimbert, L., primary, Sanz, M.N., additional, Rucker-Martin, C., additional, Novotova, M., additional, Gressette, M., additional, Gomez, S., additional, Solgadi, A., additional, Dumont, F., additional, Ventura-Clapier, R., additional, Veksler, V., additional, Piquereau, J., additional, and Garnier, A., additional
- Published
- 2019
- Full Text
- View/download PDF
9. Mitophagy induced by endoplasmic reticulum stress in heart is modulated by the sirtuin 1
- Author
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Pires Da Silva, J., primary, Monceaux, K., additional, Prola, A., additional, Ventura-Clapier, R., additional, Garnier, A., additional, and Lemaire, C., additional
- Published
- 2018
- Full Text
- View/download PDF
10. ER stress induces cardiac dysfunction through cardiomyocytes architectural modifications and alteration of mitochondrial function
- Author
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Prola, A., primary, Monceaux, K., additional, Nichtova, Z., additional, Pires Da Silva, J., additional, Piquereau, J., additional, Gressette, M., additional, Ventura-Clapier, R., additional, Garnier, A., additional, Zahradnick, I., additional, Novotova, M., additional, and Lemaire, C., additional
- Published
- 2018
- Full Text
- View/download PDF
11. SIRT1 protects the heart from endoplasmic reticulum stress-induced apoptosis through eIF2α deacetylation
- Author
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da Silva, J. Pires, primary, Prola, A., additional, Guilbert, A., additional, Lecru, L., additional, Piquereau, J., additional, Ribeiro, M., additional, Mateo, P., additional, Gressette, M., additional, Gallerne, C., additional, François, H., additional, Eid, P., additional, Ventura-Clapier, R., additional, Garnier, A., additional, and Lemaire, C., additional
- Published
- 2017
- Full Text
- View/download PDF
12. Metabolic therapy: cobalamin and folate protect mitochondrial oxidative capacity and contractile function in myocardial dysfunction
- Author
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Piquereau, J., primary, Moulin, M., additional, Zurlo, G., additional, Mateo, P., additional, Gressette, M., additional, Paul, J.L., additional, Lemaire, C., additional, Ventura-Clapier, R., additional, Veksler, V., additional, and Garnier, A., additional
- Published
- 2017
- Full Text
- View/download PDF
13. Poster session 3
- Author
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Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. L., additional, Pinho, M., additional, Pinho, S., additional, Sena, C., additional, Seica, R., additional, Leite-Moreira, A., additional, Dabroi, F., additional, Schiaffino, S., additional, Kiseleva, E., additional, Krukov, N., additional, Nikitin, O., additional, Ardatova, L., additional, Mourouzis, I., additional, Pantos, C., additional, Kokkinos, A. D., additional, Cokkinos, D. V., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M. A., additional, Pellegrino, M., additional, Calabriso, N., additional, Gastaldelli, A., additional, Storelli, C., additional, De Caterina, R., additional, Lindner, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschope, C., additional, Westermann, D., additional, Everaert, B. R., additional, Nijenhuis, V. J., additional, Reith, F. C. M., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, Vrints, C. J., additional, Simova, I., additional, Mateev, H., additional, Katova, T., additional, Haralanov, L., additional, Dimitrov, N., additional, Mironov, N., additional, Golitsyn, S. P., additional, Sokolov, S. F., additional, Yuricheva, Y. U. A., additional, Maikov, E. B., additional, Shlevkov, N. B., additional, Rosenstraukh, L. V., additional, Chazov, E. I., additional, Radosinska, J., additional, Knezl, V., additional, Benova, T., additional, Slezak, J., additional, Urban, L., additional, Tribulova, N., additional, Virag, L., additional, Kristof, A., additional, Kohajda, Z. S., additional, Szel, T., additional, Husti, Z., additional, Baczko, I., additional, Jost, N., additional, Varro, A., additional, Sarusi, A., additional, Farkas, A. S., additional, Orosz, S. Z., additional, Forster, T., additional, Farkas, A., additional, Zakhrabova-Zwiauer, O. M., additional, Hardziyenka, M., additional, Nieuwland, R., additional, Tan, H. L., additional, Raaijmakers, A. J. A., additional, Bourgonje, V. J. A., additional, Kok, G. J. M., additional, Van Veen, A. A. B., additional, Anderson, M. E., additional, Vos, M. A., additional, Bierhuizen, M. F. A., additional, Benes, J., additional, Sebestova, B., additional, Ghouri, I. A., additional, Kemi, O. J., additional, Kelly, A., additional, Burton, F. L., additional, Smith, G. L., additional, Ozdemir, S., additional, Acsai, K., additional, Doisne, N., additional, Van Der Nagel, R., additional, Beekman, H. D. M., additional, Van Veen, T. A. B., additional, Sipido, K. R., additional, Antoons, G., additional, Harmer, S. C., additional, Mohal, J. S., additional, Kemp, D., additional, Tinker, A., additional, Beech, D., additional, Burley, D. S., additional, Cox, C. D., additional, Wann, K. T., additional, Baxter, G. F., additional, Wilders, R., additional, Verkerk, A., additional, Fragkiadaki, P., additional, Germanakis, G., additional, Tsarouchas, K., additional, Tsitsimpikou, C., additional, Tsardi, M., additional, George, D., additional, Tsatsakis, A., additional, Rodrigues, P., additional, Barros, C., additional, Najmi, A. K., additional, Khan, V., additional, Akhtar, M., additional, Pillai, K. K., additional, Mujeeb, M., additional, Aqil, M., additional, Bayliss, C. R., additional, Messer, A. E., additional, Leung, M.-C., additional, Ward, D., additional, Van Der Velden, J., additional, Poggesi, C., additional, Redwood, C. S., additional, Marston, S., additional, Vite, A., additional, Gandjbakhch, E., additional, Gary, F., additional, Fressart, V., additional, Leprince, P., additional, Fontaine, G., additional, Komajda, M., additional, Charron, P., additional, Villard, E., additional, Falcao-Pires, I., additional, Gavina, C., additional, Hamdani, N., additional, Stienen, G. J. M., additional, Niessens, H. W. M., additional, Leite-Moreira, A. F., additional, Paulus, W. J., additional, Memo, M., additional, Marston, S. B., additional, Vafiadaki, E., additional, Qian, J., additional, Arvanitis, D. A., additional, Sanoudou, D., additional, Kranias, E. G., additional, Elmstedt, N., additional, Lind, B., additional, Ferm-Widlund, K., additional, Westgren, M., additional, Brodin, L.-A., additional, Mansfield, C., additional, West, T., additional, Ferenczi, M., additional, Wijnker, P. J. M., additional, Foster, D. B., additional, Coulter, A., additional, Frazier, A., additional, Murphy, A. M., additional, Shah, M., additional, Sikkel, M. B., additional, Desplantez, T., additional, Collins, T. P., additional, O' Gara, P., additional, Lyon, A. R., additional, Macleod, K. T., additional, Ottesen, A. H., additional, Louch, W. E., additional, Carlson, C., additional, Landsverk, O. J. B., additional, Stridsberg, M., additional, Sjaastad, I., additional, Oie, E., additional, Omland, T., additional, Christensen, G., additional, Rosjo, H., additional, Cartledge, J., additional, Clark, L. A., additional, Ibrahim, M., additional, Siedlecka, U., additional, Navaratnarajah, M., additional, Yacoub, M. H., additional, Camelliti, P., additional, Terracciano, C. M., additional, Chester, A., additional, Gonzalez-Tendero, A., additional, Torre, I., additional, Garcia-Garcia, F., additional, Dopazo, J., additional, Gratacos, E., additional, Taylor, D., additional, Bhandari, S., additional, Seymour, A.-M., additional, Fliegner, D., additional, Jost, J., additional, Bugger, H., additional, Ventura-Clapier, R., additional, Carpi, A., additional, Campesan, M., additional, Canton, M., additional, Menabo, R., additional, Pelicci, P. G., additional, Giorgio, M., additional, Di Lisa, F., additional, Hancock, M., additional, Venturini, A., additional, Al-Shanti, N., additional, Stewart, C., additional, Ascione, R., additional, Angelini, G., additional, Suleiman, M.-S., additional, Kravchuk, E., additional, Grineva, E., additional, Galagudza, M., additional, Kostareva, A., additional, Bairamov, A., additional, Krychtiuk, K. A., additional, Watzke, L., additional, Kaun, C., additional, Demyanets, S., additional, Pisoni, J., additional, Kastl, S. P., additional, Huber, K., additional, Maurer, G., additional, Wojta, J., additional, Speidl, W. S., additional, Varga, Z. V., additional, Farago, N., additional, Zvara, A., additional, Kocsis, G. F., additional, Pipicz, M., additional, Csonka, C., additional, Csont, T., additional, Puskas, G. L., additional, Ferdinandy, P., additional, Klevstigova, M., additional, Silhavy, J., additional, Manakov, D., additional, Papousek, F., additional, Novotny, J., additional, Pravenec, M., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Neckar, J., additional, Barallobre-Barreiro, J., additional, Didangelos, A., additional, Yin, X., additional, Fernandez-Caggiano, M., additional, Drozdov, I., additional, Willeit, P., additional, Domenech, N., additional, Mayr, M., additional, Lemoine, S., additional, Allouche, S., additional, Coulbault, L., additional, Galera, P., additional, Gerard, J. L., additional, Hanouz, J. L., additional, Suveren, E., additional, Whiteman, M., additional, Studneva, I. M., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Serebryakova, L., additional, Tskitishvili, O., additional, Timoshin, A., additional, Fauconnier, J., additional, Meli, A. C., additional, Thireau, J., additional, Roberge, S., additional, Lompre, A. M., additional, Jacotot, E., additional, Marks, A. M., additional, Lacampagne, A., additional, Dietel, B., additional, Altendorf, R., additional, Daniel, W. G., additional, Kollmar, R., additional, Garlichs, C. D., additional, Parente, V., additional, Balasso, S., additional, Pompilio, G., additional, Colombo, G., additional, Milano, G., additional, Squadroni, L., additional, Cotelli, F., additional, Pozzoli, O., additional, Capogrossi, M. C., additional, Ajiro, Y., additional, Saegusa, N., additional, Iwade, K., additional, Giles, W. R., additional, Stafforini, D. M., additional, Spitzer, K. W., additional, Sirohi, R., additional, Candilio, L., additional, Babu, G., additional, Roberts, N., additional, Lawrence, D., additional, Sheikh, A., additional, Kolvekar, S., additional, Yap, J., additional, Hausenloy, D. J., additional, Yellon, D. M., additional, Aslam, M., additional, Rohrbach, S., additional, Schlueter, K.-D., additional, Piper, H. M., additional, Noll, T., additional, Guenduez, D., additional, Malinova, L., additional, Ryabukho, V. P., additional, Lyakin, D. V., additional, Denisova, T. P., additional, Montoro-Garcia, S., additional, Shantsila, E., additional, Lip, G. Y. H., additional, Kalaska, B., additional, Sokolowska, E., additional, Kaminski, K., additional, Szczubialka, K., additional, Kramkowski, K., additional, Mogielnicki, A., additional, Nowakowska, M., additional, Buczko, W., additional, Stancheva, N., additional, Mekenyan, E., additional, Gospodinov, K., additional, Tisheva, S., additional, Darago, A., additional, Rutkai, I., additional, Kalasz, J., additional, Czikora, A., additional, Orosz, P., additional, Bjornson, H. D., additional, Edes, I., additional, Papp, Z., additional, Toth, A., additional, Riches, K., additional, Warburton, P., additional, O'regan, D. J., additional, Ball, S. G., additional, Turner, N. A., additional, Wood, I. C., additional, Porter, K. E., additional, Kogaki, S., additional, Ishida, H., additional, Nawa, N., additional, Takahashi, K., additional, Baden, H., additional, Ichimori, H., additional, Uchikawa, T., additional, Mihara, S., additional, Miura, K., additional, Ozono, K., additional, Lugano, R., additional, Padro, T., additional, Garcia-Arguinzonis, M., additional, Badimon, L., additional, Ferraro, F., additional, Viner, R., additional, Ho, J., additional, Cutler, D., additional, Matchkov, V., additional, Aalkjaer, C., additional, Krijnen, P. A. J., additional, Hahn, N. E., additional, Kholova, I., additional, Sipkens, J. A., additional, Van Alphen, F. P., additional, Simsek, S., additional, Schalkwijk, C. G., additional, Van Buul, J. D., additional, Van Hinsbergh, V. W. M., additional, Niessen, H. W. M., additional, Caro, C. G., additional, Seneviratne, A., additional, Monaco, C., additional, Hou, D., additional, Singh, J., additional, Gilson, P., additional, Burke, M. G., additional, Heraty, K. B., additional, Krams, R., additional, Coppola, G., additional, Albrecht, K., additional, Schgoer, W., additional, Wiedemann, D., additional, Bonaros, N., additional, Steger, C., additional, Theurl, M., additional, Stanzl, U., additional, Kirchmair, R., additional, Amadesi, S., additional, Spinetti, G., additional, Cangiano, E., additional, Valgimigli, M., additional, Miller, A. M., additional, Cardinali, A., additional, Vierlinger, K., additional, Pagano, G., additional, Liccardo, D., additional, Zincarelli, C., additional, Femminella, G. D., additional, Lymperopoulos, A., additional, De Lucia, C., additional, Koch, W. J., additional, Leosco, D., additional, Rengo, G., additional, Hinkel, R., additional, Husada, W., additional, Trenkwalder, T., additional, Di, Q., additional, Lee, S., additional, Petersen, B., additional, Bock-Marquette, I., additional, Niemann, H., additional, Di Maio, M., additional, Kupatt, C., additional, Nourian, M., additional, Yassin, Z., additional, Kelishadi, R., additional, Memarian, S. H., additional, Heidari, A., additional, Leuner, A., additional, Poitz, D. M., additional, Brunssen, C., additional, Ravens, U., additional, Strasser, R. H., additional, Morawietz, H., additional, Vogt, F., additional, Grahl, A., additional, Flege, C., additional, Marx, N., additional, Borinski, M., additional, De Geest, B., additional, Jacobs, F., additional, Muthuramu, I., additional, Gordts, S. C., additional, Van Craeyveld, E., additional, Herijgers, P., additional, Weinert, S., additional, Medunjanin, S., additional, Herold, J., additional, Schmeisser, A., additional, Braun-Dullaeus, R. C., additional, Wagner, A. H., additional, Moeller, K., additional, Adolph, O., additional, Schwarz, M., additional, Schwale, C., additional, Bruehl, C., additional, Nobiling, R., additional, Wieland, T., additional, Schneider, S. W., additional, Hecker, M., additional, Cross, A., additional, Strom, A., additional, Cole, J., additional, Goddard, M., additional, Hultgardh-Nilsson, A., additional, Nilsson, J., additional, Mauri, C., additional, Mitkovskaya, N. P., additional, Kurak, T. A., additional, Oganova, E. G., additional, Shkrebneva, E. I., additional, Kot, Z. H. N., additional, Statkevich, T. V., additional, Molica, F., additional, Burger, F., additional, Matter, C. M., additional, Thomas, A., additional, Staub, C., additional, Zimmer, A., additional, Cravatt, B., additional, Pacher, P., additional, Steffens, S., additional, Blanco, R., additional, Sarmiento, R., additional, Parisi, C., additional, Fandino, S., additional, Blanco, F., additional, Gigena, G., additional, Szarfer, J., additional, Rodriguez, A., additional, Garcia Escudero, A., additional, Riccitelli, M. A., additional, Wantha, S., additional, Simsekyilmaz, S., additional, Megens, R. T., additional, Van Zandvoort, M. A., additional, Liehn, E., additional, Zernecke, A., additional, Klee, D., additional, Weber, C., additional, Soehnlein, O., additional, Lima, L. M., additional, Carvalho, M. G., additional, Gomes, K. B., additional, Santos, I. R., additional, Sousa, M. O., additional, Morais, C. A. S., additional, Oliveira, S. H. V., additional, Gomes, I. F., additional, Brandao, F. C., additional, Lamego, M. R. A., additional, Fornai, L., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Heeren, R. M. A., additional, Grdinic, A., additional, Vojvodic, D., additional, Djukanovic, N., additional, Grdinic, A. G., additional, Obradovic, S., additional, Majstorovic, I., additional, Rusovic, S., additional, Vucinic, Z., additional, Tavciovski, D., additional, Ostojic, M., additional, Lai, S.-C., additional, Chen, M.-Y., additional, Wu, H.-T., additional, Gouweleeuw, L., additional, Oberdorf-Maass, S. U., additional, De Boer, R. A., additional, Van Gilst, W. H., additional, Maass, A. H., additional, Van Gelder, I. C., additional, Benard, L., additional, Li, C., additional, Warren, D., additional, Shanahan, C. M., additional, Zhang, Q. P., additional, Bye, A., additional, Vettukattil, R., additional, Aspenes, S. T., additional, Giskeodegaard, G., additional, Gribbestad, I. S., additional, Wisloff, U., additional, Bathen, T. F., additional, Cubedo, J., additional, Alonso, R., additional, Mata, P., additional, Ivic, I., additional, Vamos, Z., additional, Cseplo, P., additional, Kosa, D., additional, Torok, O., additional, Hamar, J., additional, Koller, A., additional, Norita, K., additional, De Noronha, S. V., additional, Sheppard, M. N., additional, Amat-Roldan, I., additional, Iruretagoiena, I., additional, Psilodimitrakopoulos, S., additional, Crispi, F., additional, Artigas, D., additional, Loza-Alvarez, P., additional, Harrison, J. C., additional, Smart, S. D., additional, Besely, E. H., additional, Kelly, J. R., additional, Yao, Y., additional, Sammut, I. A., additional, Hoepfner, M., additional, Kuzyniak, W., additional, Sekhosana, E., additional, Hoffmann, B., additional, Litwinski, C., additional, Pries, A., additional, Ermilov, E., additional, Fontoura, D., additional, Lourenco, A. P., additional, Vasques-Novoa, F., additional, Pinto, J. P., additional, Roncon-Albuquerque, R., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Usman, T. O., additional, Olatunji, V. A., additional, Bacova, B., additional, Viczenczova, C., additional, Dosenko, V., additional, Goncalvesova, E., additional, Vanrooyen, J., additional, Maulik, S. K., additional, Seth, S., additional, Dinda, A. K., additional, Jaiswal, A., additional, Mearini, G., additional, Khajetoorians, D., additional, Kraemer, E., additional, Gedicke-Hornung, C., additional, Precigout, G., additional, Eschenhagen, T., additional, Voit, T., additional, Garcia, L., additional, Lorain, S., additional, Mendes-Ferreira, P., additional, Maia-Rocha, C., additional, Adao, R., additional, Cerqueira, R. J., additional, Mendes, M. J., additional, Castro-Chaves, P., additional, De Keulenaer, G. W., additional, Bras-Silva, C., additional, Ruiter, G., additional, Wong, Y. Y., additional, Lubberink, M., additional, Knaapen, P., additional, Raijmakers, P., additional, Lammertsma, A. A., additional, Marcus, J. T., additional, Westerhof, N., additional, Van Der Laarse, W. J., additional, Vonk-Noordegraaf, A., additional, Steinbronn, N., additional, Koch, E., additional, Steiner, G., additional, Berezin, A., additional, Lisovaya, O. A., additional, Soldatova, A. M., additional, Kuznetcov, V. A., additional, Yenina, T. N., additional, Rychkov, A. Y. U., additional, Shebeko, P. V., additional, Altara, R., additional, Hessel, M. H. M., additional, Hermans, J. J. R., additional, Blankesteijn, W. M., additional, Berezina, T. A., additional, Seden, V., additional, Bonanad, C., additional, Nunez, J., additional, Navarro, D., additional, Chilet, M. F., additional, Sanchis, F., additional, Bodi, V., additional, Minana, G., additional, Chaustre, F., additional, Forteza, M. J., additional, Llacer, A., additional, Galasso, G., additional, Ferrara, N., additional, Akhmedov, A., additional, Klingenberg, R., additional, Brokopp, C., additional, Hof, D., additional, Zoller, S., additional, Corti, R., additional, Gay, S., additional, Von Eckardstein, A., additional, Hoerstrup, S. P., additional, Luescher, T. F., additional, Heijman, J., additional, Zaza, A., additional, Johnson, D. M., additional, Rudy, Y., additional, Peeters, R. L. M., additional, Volders, P. G. A., additional, Westra, R. L., additional, Fujita, S., additional, Okamoto, R., additional, Taniguchi, M., additional, Konishi, K., additional, Goto, I., additional, Sugimoto, K., additional, Nakamura, M., additional, Shiraki, K., additional, Buechler, C., additional, and Ito, M., additional
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- 2012
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14. Poster session 2
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Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. 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S., additional, Rocchiccioli, S., additional, Cecchettini, A., additional, Pelosi, G., additional, Citti, L., additional, Parodi, O., additional, Trivella, M. G., additional, Michel-Monigadon, D., additional, Burger, F., additional, Dunoyer-Geindre, S., additional, Pelli, G., additional, Cravatt, B., additional, Steffens, S., additional, Didangelos, A., additional, Mayr, U., additional, Yin, X., additional, Stegemann, C., additional, Shalhoub, J., additional, Davies, A. H., additional, Monaco, C., additional, Mayr, M., additional, Lypovetska, S., additional, Grytsenko, S., additional, Njerve, I. U., additional, Pettersen, A. A., additional, Opstad, T. B., additional, Bratseth, V., additional, Arnesen, H., additional, Seljeflot, I., additional, Dumitriu, I. E., additional, Baruah, P., additional, Antunes, R. F., additional, Kaski, J. C., additional, Trapero, I., additional, Benet, I., additional, Alguero, C., additional, Chaustre, F. J., additional, Mangold, A., additional, Puthenkalam, S., additional, Distelmaier, K., additional, Adlbrecht, C., additional, Lang, I. M., additional, Koizumi, T., additional, Inoue, I., additional, Komiyama, N., additional, Nishimura, S., additional, Korneeva, O. N., additional, Drapkina, O. M., additional, Fornai, L., additional, Angelini, A., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Thiene, G., additional, Heeren, R. M. A., additional, Padro, T., additional, Casani, L., additional, Suades, R., additional, Bertoni, B., additional, Carminati, R., additional, Carlini, V., additional, Pettinari, L., additional, Martinelli, C., additional, Gagliano, N., additional, Noppe, G., additional, Buchlin, P., additional, Marquet, N., additional, Baeyens, N., additional, Morel, N., additional, Baysa, A., additional, Sagave, J., additional, Dahl, C. P., additional, Gullestad, L., additional, Carpi, A., additional, Di Lisa, F., additional, Giorgio, M., additional, Vaage, J., additional, Valen, G., additional, Vafiadaki, E., additional, Papalouka, V., additional, Terzis, G., additional, Spengos, K., additional, Manta, P., additional, Gales, C., additional, Genet, G., additional, Dague, E., additional, Cazorla, O., additional, Payre, B., additional, Mias, C., additional, Ouille, A., additional, Lacampagne, A., additional, Pathak, A., additional, Senard, J. M., additional, Abonnenc, M., additional, Da Costa Martins, P., additional, Srivastava, S., additional, Gautel, M., additional, De Windt, L., additional, Comelli, L., additional, Lande, C., additional, Ucciferri, N., additional, Ikonen, L., additional, Vuorenpaa, H., additional, Kujala, K., additional, Sarkanen, J.-R., additional, Heinonen, T., additional, Ylikomi, T., additional, Aalto-Setala, K., additional, Capros, H., additional, Sprincean, N., additional, Usurelu, N., additional, Egorov, V., additional, Stratu, N., additional, Matchkov, V., additional, Bouzinova, E., additional, Moeller-Nielsen, N., additional, Wiborg, O., additional, Gutierrez, P. S., additional, Aparecida-Silva, R., additional, Borges, L. F., additional, Moreira, L. F. P., additional, Dias, R. R., additional, Kalil, J., additional, Stolf, N. A. G., additional, Zhou, W., additional, Suntharalingam, K., additional, Brand, N., additional, Vilar Compte, R., additional, Ying, L., additional, Bicknell, K., additional, Dannoura, A., additional, Dash, P., additional, Brooks, G., additional, Tsimafeyeu, I., additional, Tishova, Y., additional, Wynn, N., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Maegdefessel, L., additional, Azuma, J., additional, Toh, R., additional, Raaz, U., additional, Merk, D. R., additional, Deng, A., additional, Spin, J. M., additional, Tsao, P. S., additional, Tedeschi, L., additional, Taranta, M., additional, Naldi, I., additional, Grimaldi, S., additional, Cinti, C., additional, Bousquenaud, M., additional, Maskali, F., additional, Poussier, S., additional, Marie, P. Y., additional, Boutley, H., additional, Karcher, G., additional, Wagner, D. R., additional, Devaux, Y., additional, Torre, I., additional, Psilodimitrakopoulos, S., additional, Iruretagoiena, I., additional, Gonzalez-Tendero, A., additional, Artigas, D., additional, Loza-Alvarez, P., additional, Gratacos, E., additional, Amat-Roldan, I., additional, Murray, L., additional, Carberry, D. M., additional, Dunton, P., additional, Miles, M. J., additional, Suleiman, M.-S., additional, Kanesalingam, K., additional, Taylor, R., additional, Mc Collum, C. N., additional, Parniczky, A., additional, Solymar, M., additional, Porpaczy, A., additional, Miseta, A., additional, Lenkey, Z. S., additional, Szabados, S., additional, Cziraki, A., additional, Garai, J., additional, Myloslavska, I., additional, Menazza, S. M., additional, Canton, M. C., additional, Di Lisa, F. D. L., additional, Oliveira, S. H. V., additional, Morais, C. A. S., additional, Miranda, M. R., additional, Oliveira, T. T., additional, Lamego, M. R. A., additional, Lima, L. M., additional, Goncharova, N. S., additional, Naymushin, A. V., additional, Kazimli, A. V., additional, Moiseeva, O. M., additional, Carvalho, M. G., additional, Sabino, A. P., additional, Mota, A. P. L., additional, Sousa, M. O., additional, Niessner, A., additional, Richter, B., additional, Hohensinner, P. J., additional, Rychli, K., additional, Zorn, G., additional, Berger, R., additional, Moertl, D., additional, Pacher, R., additional, Wojta, J., additional, Huelsmann, M., additional, Kukharchik, G., additional, Nesterova, N., additional, Pavlova, A., additional, Gaykovaya, L., additional, Krapivka, N., additional, Konstantinova, I., additional, Sichinava, L., additional, Prapa, S., additional, Mccarthy, K. P., additional, Kilner, P. J., additional, Xu, X. Y., additional, Johnson, M. R., additional, Ho, S. Y., additional, Gatzoulis, M. A., additional, Stoupel, E. G., additional, Garcia, R., additional, Merino, D., additional, Montalvo, C., additional, Hurle, M. A., additional, Nistal, J. F., additional, Villar, A. V., additional, Perez-Moreno, A., additional, Gilabert, R., additional, and Ros, E., additional
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- 2012
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15. Muscle creatine kinase-deficient mice: II cardiac and skeletal muscles exhibit tissue-specific adaption of the mitochondrial function
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Veksler, V.I., Kuznetsov, A.V., Anflous, K., Mateo, P., Deursen, J.M.A. van, Wieringa, B., and Ventura-Clapier, R.
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Targeted insertional mutagenesis in chromosomal DNA of cell lines and the germ line of mice as means to study gene function ,Gerichte mutagenese in chromosomaal DNA van cellijnen en de kiembaan van muizen als middel voor bestudering van genfunctie - Abstract
Contains fulltext : 174479.pdf (Publisher’s version ) (Open Access)
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- 1995
16. Muscle creatine kinase-deficient mice
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Ventura-Clapier, R., Kuznetsov, A.V., Albis, A. d', Deursen, J.M.A. van, Wieringa, B., and Veksler, V.I.
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GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries) - Abstract
Contains fulltext : 20682___.PDF (Publisher’s version ) (Open Access)
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- 1995
17. Mitochondria as a source of mechanical signals in cardiomyocytes
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Kaasik, A., primary, Kuum, M., additional, Joubert, F., additional, Wilding, J., additional, Ventura-Clapier, R., additional, and Veksler, V., additional
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- 2010
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18. Energetic state is a strong regulator of sarcoplasmic reticulum Ca2+ loss in cardiac muscle: different efficiencies of different energy sources
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Kuum, M., primary, Kaasik, A., additional, Joubert, F., additional, Ventura-Clapier, R., additional, and Veksler, V., additional
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- 2009
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19. B011 Stimulus specific changes of energy metabolism in hypertrophied heart
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Rimbaud, S., primary, Sanchez, H., additional, Garnier, A., additional, Fortin, D., additional, Bigard, X., additional, Veksler, V., additional, and Ventura-Clapier, R., additional
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- 2009
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20. C013 Cocaine-induced LV diastolic impairment is associated with cardiac mitochondrial dysfunction and ROS production: role of nadph and xanthine oxidase
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Vergeade, A., primary, Mulder, P., additional, Dehaudt, C., additional, Fortin, D., additional, Ventura-Clapier, R., additional, Thuillez, C., additional, and Monteil, C., additional
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- 2009
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21. J015 Rôle de l’architecture cellulaire dans la signalisation énergétique du cœur de souris au cours du développement postnatal
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Piquereau, J., primary, Joubert, F., additional, Fortin, D., additional, Novotova, M., additional, Ventura-Clapier, R., additional, and Veksler, V., additional
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- 2009
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22. Transcriptional control of mitochondrial biogenesis: the central role of PGC-1
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Ventura-Clapier, R., primary, Garnier, A., additional, and Veksler, V., additional
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- 2008
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23. Mitochondrial biogenesis in fast skeletal muscle of CK deficient mice
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Vaarmann, A., primary, Fortin, D., additional, Veksler, V., additional, Momken, I., additional, Ventura-Clapier, R., additional, and Garnier, A., additional
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- 2008
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24. Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?
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Bahi, L., primary, Koulmann, N., additional, Sanchez, H., additional, Momken, I., additional, Veksler, V., additional, Bigard, A. X., additional, and Ventura-Clapier, R., additional
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- 2004
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25. Errata
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Garnier, A., primary, Fortin, D., additional, Deloménie, C., additional, Momken, I., additional, Veksler, V., additional, and Ventura‐Clapier, R., additional
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- 2003
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26. Depressed mitochondrial transcription factors and oxidative capacity in rat failing cardiac and skeletal muscles
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Garnier, A., primary, Fortin, D., additional, Deloménie, C., additional, Momken, I., additional, Veksler, V., additional, and Ventura‐Clapier, R., additional
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- 2003
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27. Physical activity changes the regulation of mitochondrial respiration in human skeletal muscle
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Zoll, J., primary, Sanchez, H., additional, N'Guessan, B., additional, Ribera, F., additional, Lampert, E., additional, Bigard, X., additional, Serrurier, B., additional, Fortin, D., additional, Geny, B., additional, Veksler, V., additional, Ventura‐Clapier, R., additional, and Mettauer, B., additional
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- 2002
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28. Influence of overload on phenotypic remodeling in regenerated skeletal muscle
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Bigard, A. X., primary, Zoll, J., additional, Ribera, F., additional, Mateo, P., additional, Sanchez, H., additional, Serrurier, B., additional, and Ventura-Clapier, R., additional
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- 2001
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29. Effect of cyclosporin A and its vehicle on cardiac and skeletal muscle mitochondria: relationship to efficacy of the respiratory chain
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Sanchez, H, primary, Zoll, J, additional, Bigard, X, additional, Veksler, V, additional, Mettauer, B, additional, Lampert, E, additional, Lonsdorfer, J, additional, and Ventura-Clapier, R, additional
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- 2001
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30. Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle
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De Sousa, E., primary, Veksler, V., additional, Bigard, X., additional, Mateo, P., additional, and Ventura-Clapier, R., additional
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- 2000
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31. Subcellular Creatine Kinase Alterations
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De Sousa, E., primary, Veksler, V., additional, Minajeva, A., additional, Kaasik, A., additional, Mateo, P., additional, Mayoux, E., additional, Hoerter, J., additional, Bigard, X., additional, Serrurier, B., additional, and Ventura-Clapier, R., additional
- Published
- 1999
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32. Myocardial ischemic contracture. Metabolites affect rigor tension development and stiffness.
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Ventura-Clapier, R, primary and Veksler, V, additional
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- 1994
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33. Mechanical properties of rat cardiac skinned fibers are altered by chronic growth hormone hypersecretion.
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Mayoux, E, primary, Ventura-Clapier, R, additional, Timsit, J, additional, Béhar-Cohen, F, additional, Hoffmann, C, additional, and Mercadier, J J, additional
- Published
- 1993
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34. Functional development of the creatine kinase system in perinatal rabbit heart.
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Hoerter, J A, primary, Kuznetsov, A, additional, and Ventura-Clapier, R, additional
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- 1991
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35. Neurohormonal control of calcium sensitivity of myofilaments in rat single heart cells.
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Puceat, M, primary, Clement, O, additional, Lechene, P, additional, Pelosin, J M, additional, Ventura-Clapier, R, additional, and Vassort, G, additional
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- 1990
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36. Compartmentation of creatine kinase isoenzymes in myometrium of gravid guinea‐pig.
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Clark, J F, Khuchua, Z, Kuznetsov, A, Saks, V A, and Ventura‐Clapier, R
- Abstract
1. This study was performed to investigate the possible presence and role of the creatine kinase (CK) system in the contraction and relaxation of skinned guinea‐pig uterus as well as the changes of the CK system during gestation. Experiments were performed on isolated longitudinal fibres of gravid and non‐gravid myometrium. 2. Total CK activity increased from 74 +/‐ 11 to 196 +/‐ 39 IU (g wet wt)‐1 during gestation. 3. The four isoenzymes of CK: muscle (MM), muscle‐brain (MB), brain (BB) and mitochondrial (mt‐CK) were found in myometrium. MM, MB and BB isoenzymes represented respectively 20.3 +/‐ 2.6, 10.3 +/‐ 4.4 and 72.7 +/‐ 2.2% of total activity. The distribution of isoenzymes did not significantly change with gestation, the contribution of mt‐CK increasing from trace to 5% of total activity. 4. BB‐CK was specifically bound to Triton X‐100‐skinned fibres with the non‐gravid uterus containing 6.7 +/‐ 1.9 IU (g wet wt)‐1 and the gravid uterus containing 44 +/‐ 13 IU (g wet wt)‐1. 5. Active tension of Triton X‐100‐treated fibres increased from 6.06 +/‐ 0.68 to 19.3 +/‐ 1.9 mM mm‐2 during gestation. 6. Submaximal tension (43.3 +/‐ 4.4% of maximal tension) can be developed in the absence of ATP and in the presence of 12 mM phosphocreatine (PCr) and 250 microM MgADP from endogenous CK in non‐gravid uterine fibres while the gravid uterus was able to generate 65.4 +/‐ 3.9% of maximal tension via the CK system. 7. The endogenous CK system was able to relax the skinned fibres from high‐tension rigor conditions by 47.3 +/‐ 4.2% of total relaxation in non‐gravid fibres and 60.6 +/‐ 3.2% of total relaxation in gravid fibres. 8. Non‐gravid and gravid uteri both contained mt‐CK of 17.5 +/‐ 8.4 and 140 +/‐ 22 micrograms (g wet wt)‐1 respectively as determined with antibodies against mt‐CK. 9. Oxygen consumption was studied in fibres where the plasmalemma was solubilized with 50 micrograms ml‐1 saponin. Maximal respiration was increased from 0.91 +/‐ 0.05 to 2.61 +/‐ 0.16 mumol oxygen min‐1 (g dry wt)‐1 in the gravid uterine fibres. However, creatine did not stimulate respiration in the uterine fibres treated with saponin. 10. It is concluded that the CK system undergoes qualitative as well as quantitative changes during gestation. BB‐CK is specifically localized in the myofilaments and mt‐CK is present in the uterine mitochondria.(ABSTRACT TRUNCATED AT 400 WORDS)
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- 1993
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37. Role of creatine kinase in force development in chemically skinned rat cardiac muscle.
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Ventura-Clapier, R, Mekhfi, H, and Vassort, G
- Abstract
The influence of phosphocreatine in the presence or absence of MgATP and MgADP was studied in Triton X-100-treated thin papillary muscles and ventricular strips of the rat heart. The pCa/tension relationships, the pMgATP/tension relationships, and the tension responses to quick length changes were analyzed. The results show three major consequences of the reduction of the phosphocreatine concentration in the presence of millimolar concentrations of the MgATP. (a) The resting tension and the maximal Ca2+-activated tension were increased, and the pCa/tension relationship was shifted toward higher pCa values and its steepness was decreased; these effects were enhanced by the inclusion of MgADP. (b) The time constant of tension recoveries after quick stretches applied during maximal activation was increased, while the extent of these recoveries was decreased. (c) The study of pMgATP/tension relationships in low Ca concentrations showed that the decrease in phosphocreatine induced a shift toward higher MgATP values with no changes in maximal rigor tension or the slope coefficient; these effects were increased by the increase in MgADP and were independent of the preparation diameter. Thus, modifications of the apparent Ca sensitivity and resting and maximal tension when phosphocreatine is decreased seem to be due to an increasing participation of rigor-like or slowly cycling cross-bridges spending more time in the attached state. These results suggest that endogenous creatine kinase is able to ensure maximal efficiency of myosin ATPase by producing a local high MgATP/MgADP ratio.
- Published
- 1987
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38. Creatine kinase in regulation of heart function and metabolism. I. Further evidence for compartmentation of adenine nucleotides in cardiac myofibrillar and sarcolemmal coupled ATPase-creatine kinase systems
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Saks, V.A., primary, Ventura-Clapier, R., additional, Huchua, Z.A., additional, Preobrazhensky, A.N., additional, and Emelin, I.V., additional
- Published
- 1984
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39. EFFECTS OF HALOTHANE AND ISOFLURANE ON CONTRACTILE PROPERTIES OF BABY AND ADULT RABBIT CARDIAC SKINNED FIBERS
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MURAT, I, primary, HOERTER, J, additional, and VENTURA-CLAPIER, R, additional
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- 1989
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40. HALOTHANE, ENFLURANE AND ISOFLURANE DECREASE MYOFIBRILLAR CALCIUM SENSITIVITY IN CHEMICALLY SKINNED CARDIAC FIBERS
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Murat, I., primary, Ventura-Clapier, R., additional, and Vassort, G., additional
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- 1988
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41. Nitric oxide inhibits cardiac energy production via inhibition of mitochondrial creatine kinase
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Kaasik, A., Minajeva, A., Sousa, E. De, Ventura-Clapier, R., and Veksler, V.
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- 1999
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42. 352 - Metabolic therapy: cobalamin and folate protect mitochondrial oxidative capacity and contractile function in myocardial dysfunction.
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Piquereau, J., Moulin, M., Zurlo, G., Mateo, P., Gressette, M., Paul, J.L., Lemaire, C., Ventura-Clapier, R., Veksler, V., and Garnier, A.
- Published
- 2017
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43. 045 - SIRT1 protects the heart from endoplasmic reticulum stress-induced apoptosis through eIF2α deacetylation.
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da Silva, J. Pires, Prola, A., Guilbert, A., Lecru, L., Piquereau, J., Ribeiro, M., Mateo, P., Gressette, M., Gallerne, C., François, H., Eid, P., Ventura-Clapier, R., Garnier, A., and Lemaire, C.
- Published
- 2017
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44. Modulation of cardiac cAMP signaling by AMPK and its adjustments in pressure overload-induced myocardial dysfunction in rat and mouse.
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Garnier A, Leroy J, Deloménie C, Mateo P, Viollet B, Veksler V, Mericskay M, Ventura-Clapier R, and Piquereau J
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- Mice, Rats, Animals, Calcium, Myocytes, Cardiac, Adrenergic Agents, Calcium, Dietary, AMP-Activated Protein Kinases, Heart Failure
- Abstract
The beta-adrenergic system is a potent stimulus for enhancing cardiac output that may become deleterious when energy metabolism is compromised as in heart failure. We thus examined whether the AMP-activated protein kinase (AMPK) that is activated in response to energy depletion may control the beta-adrenergic pathway. We studied the cardiac response to beta-adrenergic stimulation of AMPKα2-/- mice or to pharmacological AMPK activation on contractile function, calcium current, cAMP content and expression of adenylyl cyclase 5 (AC5), a rate limiting step of the beta-adrenergic pathway. In AMPKα2-/- mice the expression of AC5 (+50%), the dose response curve of left ventricular developed pressure to isoprenaline (p<0.001) or the response to forskolin, an activator of AC (+25%), were significantly increased compared to WT heart. Similarly, the response of L-type calcium current to 3-isobutyl-l-methylxanthine (IBMX), a phosphodiesterase inhibitor was significantly higher in KO (+98%, p<0.01) than WT (+57%) isolated cardiomyocytes. Conversely, pharmacological activation of AMPK by 5-aminoimidazole-4-carboxamide riboside (AICAR) induced a 45% decrease in AC5 expression (p<0.001) and a 40% decrease of cAMP content (P<0.001) as measured by fluorescence resonance energy transfer (FRET) compared to unstimulated rat cardiomyocytes. Finally, in experimental pressure overload-induced cardiac dysfunction, AMPK activation was associated with a decreased expression of AC5 that was blunted in AMPKα2-/- mice. The results show that AMPK activation down-regulates AC5 expression and blunts the beta-adrenergic cascade. This crosstalk between AMPK and beta-adrenergic pathways may participate in a compensatory energy sparing mechanism in dysfunctional myocardium., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Garnier et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
- Published
- 2023
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45. Ferulic Acid, Pterostilbene, and Tyrosol Protect the Heart from ER-Stress-Induced Injury by Activating SIRT1-Dependent Deacetylation of eIF2α.
- Author
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Monceaux K, Gressette M, Karoui A, Pires Da Silva J, Piquereau J, Ventura-Clapier R, Garnier A, Mericskay M, and Lemaire C
- Subjects
- Animals, Apoptosis, Coumaric Acids, Endoplasmic Reticulum Stress, Mice, Phenylethyl Alcohol analogs & derivatives, Stilbenes, Unfolded Protein Response, eIF-2 Kinase metabolism, Eukaryotic Initiation Factor-2 metabolism, Sirtuin 1 metabolism
- Abstract
Disturbances in Endoplasmic Reticulum (ER) homeostasis induce ER stress, which has been involved in the development and progression of various heart diseases, including arrhythmias, cardiac hypertrophy, ischemic heart diseases, dilated cardiomyopathy, and heart failure. A mild-to-moderate ER stress is considered beneficial and adaptative for heart functioning by engaging the pro-survival unfolded protein response (UPR) to restore normal ER function. By contrast, a severe or prolonged ER stress is detrimental by promoting cardiomyocyte apoptosis through hyperactivation of the UPR pathways. Previously, we have demonstrated that the NAD
+ -dependent deacetylase SIRT1 is cardioprotective in response to severe ER stress by regulating the PERK pathway of the UPR, suggesting that activation of SIRT1 could protect against ER-stress-induced cardiac damage. The purpose of this study was to identify natural molecules able to alleviate ER stress and inhibit cardiomyocyte cell death through SIRT1 activation. Several phenolic compounds, abundant in vegetables, fruits, cereals, wine, and tea, were reported to stimulate the deacetylase activity of SIRT1. Here, we evaluated the cardioprotective effect of ten of these phenolic compounds against severe ER stress using cardiomyoblast cells and mice. Among the molecules tested, we showed that ferulic acid, pterostilbene, and tyrosol significantly protect cardiomyocytes and mice heart from cardiac alterations induced by severe ER stress. By studying the mechanisms involved, we showed that the activation of the PERK/eIF2α/ATF4/CHOP pathway of the UPR was reduced by ferulic acid, pterostilbene, and tyrosol under ER stress conditions, leading to a reduction in cardiomyocyte apoptosis. The protection afforded by these phenolic compounds was not directly related to their antioxidant activity but rather to their ability to increase SIRT1-mediated deacetylation of eIF2α. Taken together, our results suggest that ferulic acid, pterostilbene, and tyrosol are promising molecules to activate SIRT1 to protect the heart from the adverse effects of ER stress.- Published
- 2022
- Full Text
- View/download PDF
46. Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?
- Author
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Piquereau J, Boitard SE, Ventura-Clapier R, and Mericskay M
- Subjects
- Animals, Dietary Supplements, Energy Metabolism drug effects, Humans, Myocardium metabolism, Heart Failure drug therapy, Heart Failure metabolism, Metabolic Diseases drug therapy, Metabolic Diseases metabolism, Vitamin B Complex pharmacology
- Abstract
Heart failure (HF) is a plague of the aging population in industrialized countries that continues to cause many deaths despite intensive research into more effective treatments. Although the therapeutic arsenal to face heart failure has been expanding, the relatively short life expectancy of HF patients is pushing towards novel therapeutic strategies. Heart failure is associated with drastic metabolic disorders, including severe myocardial mitochondrial dysfunction and systemic nutrient deprivation secondary to severe cardiac dysfunction. To date, no effective therapy has been developed to restore the cardiac energy metabolism of the failing myocardium, mainly due to the metabolic complexity and intertwining of the involved processes. Recent years have witnessed a growing scientific interest in natural molecules that play a pivotal role in energy metabolism with promising therapeutic effects against heart failure. Among these molecules, B vitamins are a class of water soluble vitamins that are directly involved in energy metabolism and are of particular interest since they are intimately linked to energy metabolism and HF patients are often B vitamin deficient. This review aims at assessing the value of B vitamin supplementation in the treatment of heart failure.
- Published
- 2021
- Full Text
- View/download PDF
47. Spatiotemporal AMPKα2 deletion in mice induces cardiac dysfunction, fibrosis and cardiolipin remodeling associated with mitochondrial dysfunction in males only.
- Author
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Grimbert L, Sanz MN, Gressette M, Rucker-Martin C, Novotova M, Solgadi A, Karoui A, Gomez S, Bedouet K, Jacquet E, Lemaire C, Veksler V, Mericskay M, Ventura-Clapier R, Piquereau J, and Garnier A
- Subjects
- Animals, Female, Fibrosis, Male, Mice, Mice, Knockout, Mitochondria, Cardiolipins, Heart Diseases
- Abstract
Background: The AMP-activated protein kinase (AMPK) is a major regulator of cellular energetics which plays key role in acute metabolic response and in long-term adaptation to stress. Recent works have also suggested non-metabolic effects., Methods: To decipher AMPK roles in the heart, we generated a cardio-specific inducible model of gene deletion of the main cardiac catalytic subunit of AMPK (Ampkα2) in mice. This allowed us to avoid the eventual impact of AMPK-KO in peripheral organs., Results: Cardio-specific Ampkα2 deficiency led to a progressive left ventricular systolic dysfunction and the development of cardiac fibrosis in males. We observed a reduction in complex I-driven respiration without change in mitochondrial mass or in vitro complex I activity, associated with a rearrangement of the cardiolipins and reduced integration of complex I into the electron transport chain supercomplexes. Strikingly, none of these defects were present in females. Interestingly, suppression of estradiol signaling by ovariectomy partially mimicked the male sensitivity to AMPK loss, notably the cardiac fibrosis and the rearrangement of cardiolipins, but not the cardiac function that remained protected., Conclusion: Our results confirm the close link between AMPK and cardiac mitochondrial function, but also highlight links with cardiac fibrosis. Importantly, we show that AMPK is differently involved in these processes in males and females, which may have clinical implications for the use of AMPK activators in the treatment of heart failure., (© 2021. The Author(s).)
- Published
- 2021
- Full Text
- View/download PDF
48. Energetic Interactions Between Subcellular Organelles in Striated Muscles.
- Author
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Piquereau J, Veksler V, Novotova M, and Ventura-Clapier R
- Abstract
Adult striated muscle cells present highly organized structure with densely packed intracellular organelles and a very sparse cytosol accounting for only few percent of cell volume. These cells have a high and fluctuating energy demand that, in continuously working oxidative muscles, is fulfilled mainly by oxidative metabolism. ATP produced by mitochondria should be directed to the main energy consumers, ATPases of the excitation-contraction system; at the same time, ADP near ATPases should rapidly be eliminated. This is achieved by phosphotransfer kinases, the most important being creatine kinase (CK). Specific CK isoenzymes are located in mitochondria and in close proximity to ATPases, forming efficient energy shuttle between these structures. In addition to phosphotransfer kinases, ATP/ADP can be directly channeled between mitochondria co-localized with ATPases in a process called "direct adenine nucleotide channeling, DANC." This process is highly plastic so that inactivation of the CK system increases the participation of DANC to energy supply owing to the rearrangement of cell structure. The machinery for DANC is built during postnatal development in parallel with the increase in mitochondrial mass, organization, and complexification of the cell structure. Disorganization of cell architecture remodels the mitochondrial network and decreases the efficacy of DANC, showing that this process is intimately linked to cardiomyocyte structure. Accordingly, in heart failure, disorganization of the cell structure along with decrease in mitochondrial mass reduces the efficacy of DANC and together with alteration of the CK shuttle participates in energetic deficiency contributing to contractile failure., (Copyright © 2020 Piquereau, Veksler, Novotova and Ventura-Clapier.)
- Published
- 2020
- Full Text
- View/download PDF
49. SIRT1 Protects the Heart from ER Stress-Induced Injury by Promoting eEF2K/eEF2-Dependent Autophagy.
- Author
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Pires Da Silva J, Monceaux K, Guilbert A, Gressette M, Piquereau J, Novotova M, Ventura-Clapier R, Garnier A, and Lemaire C
- Subjects
- Animals, Elongation Factor 2 Kinase antagonists & inhibitors, Elongation Factor 2 Kinase genetics, Heat-Shock Proteins metabolism, Isoproterenol pharmacology, Mice, Mice, Inbred C57BL, Mice, Knockout, Microtubule-Associated Proteins metabolism, Myocytes, Cardiac cytology, Myocytes, Cardiac metabolism, RNA Interference, RNA, Small Interfering metabolism, Rats, Sequestosome-1 Protein metabolism, Signal Transduction drug effects, Sirtuin 1 antagonists & inhibitors, Sirtuin 1 genetics, Tunicamycin pharmacology, Autophagy drug effects, Elongation Factor 2 Kinase metabolism, Endoplasmic Reticulum Stress drug effects, Sirtuin 1 metabolism
- Abstract
Many recent studies have demonstrated the involvement of endoplasmic reticulum (ER) stress in the development of cardiac diseases and have suggested that modulation of ER stress response could be cardioprotective. Previously, we demonstrated that the deacetylase Sirtuin 1 (SIRT1) attenuates ER stress response and promotes cardiomyocyte survival. Here, we investigated whether and how autophagy plays a role in SIRT1-afforded cardioprotection against ER stress. The results revealed that protective autophagy was initiated before cell death in response to tunicamycin (TN)-induced ER stress in cardiac cells. SIRT1 inhibition decreased ER stress-induced autophagy, whereas its activation enhanced autophagy. In response to TN- or isoproterenol-induced ER stress, mice deficient for SIRT1 exhibited suppressed autophagy along with exacerbated cardiac dysfunction. At the molecular level, we found that in response to ER stress (i) the extinction of eEF2 or its kinase eEF2K not only reduced autophagy but further activated cell death, (ii) inhibition of SIRT1 inhibited the phosphorylation of eEF2, (iii) eIF2α co-immunoprecipitated with eEF2K, and (iv) knockdown of eIF2α reduced the phosphorylation of eEF2. Our results indicate that in response to ER stress, SIRT1 activation promotes cardiomyocyte survival by enhancing autophagy at least through activation of the eEF2K/eEF2 pathway., Competing Interests: The authors declare no conflict of interest.
- Published
- 2020
- Full Text
- View/download PDF
50. Inducible Cardiac-Specific Deletion of Sirt1 in Male Mice Reveals Progressive Cardiac Dysfunction and Sensitization of the Heart to Pressure Overload.
- Author
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Sanz MN, Grimbert L, Moulin M, Gressette M, Rucker-Martin C, Lemaire C, Mericskay M, Veksler V, Ventura-Clapier R, Garnier A, and Piquereau J
- Subjects
- Animals, Echocardiography, Fibrosis pathology, Gene Deletion, Heart Diseases metabolism, Heart Diseases pathology, Male, Mice, Mice, Knockout, Mitochondria metabolism, Myocytes, Cardiac, Oxidative Stress, Reactive Oxygen Species, Tamoxifen adverse effects, Heart, Heart Diseases genetics, Pressure, Sirtuin 1 genetics, Sirtuin 1 metabolism
- Abstract
Heart failure is associated with profound alterations of energy metabolism thought to play a major role in the progression of this syndrome. SIRT1 is a metabolic sensor of cellular energy and exerts essential functions on energy metabolism, oxidative stress response, apoptosis, or aging. Importantly, SIRT1 deacetylates the peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α), the master regulator of energy metabolism involved in mitochondrial biogenesis and fatty acid utilization. However, the exact role of SIRT1 in controlling cardiac energy metabolism is still incompletely understood and conflicting results have been obtained. We generated a cardio-specific inducible model of Sirt1 gene deletion in mice ( Sirt1
ciKO ) to decipher the role of SIRT1 in control conditions and following cardiac stress induced by pressure overload. SIRT1 deficiency induced a progressive cardiac dysfunction, without overt alteration in mitochondrial content or properties. Sixteen weeks after Sirt1 deletion an increase in mitochondrial reactive oxygen species (ROS) production and a higher rate of oxidative damage were observed, suggesting disruption of the ROS production/detoxification balance. Following pressure overload, cardiac dysfunction and alteration in mitochondrial properties were exacerbated in Sirt1ciKO mice. Overall the results demonstrate that SIRT1 plays a cardioprotective role on cardiac energy metabolism and thereby on cardiac function.- Published
- 2019
- Full Text
- View/download PDF
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