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101. Erratum to: Transcriptome and proteome mapping in the sheep atria reveal molecular features of atrial fibrillation progression

Author

Alvarez-Franco, Alba, primary, Rouco, Raquel, additional, Ramirez, Rafael J, additional, Guerrero-Serna, Guadalupe, additional, Tiana, Maria, additional, Cogliati, Sara, additional, Kaur, Kuljeet, additional, Saeed, Mohammed, additional, Magni, Ricardo, additional, Enriquez, Jose Antonio, additional, Sanchez-Cabo, Fatima, additional, Jalife, José, additional, and Manzanares, Miguel, additional

Published
2021
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102. Dual Dysfunction of Kir2.1 Underlies Conduction and Excitation-Contraction Coupling Defects Promoting Arrhythmias in a Mouse Model of Andersen-Tawil Syndrome Type 1

Author

Macías, Álvaro, primary, González-Guerra, Andrés, additional, Moreno-Manuel, Ana I., additional, Cruz, Francisco M., additional, García-Quintáns, Nieves, additional, Gutiérrez, Lilian K., additional, Roche-Molina, Marta, additional, Bermúdez-Jiménez, Francisco, additional, Andrés, Vicente, additional, Vera-Pedrosa, María Linarejos, additional, Martínez-Carrascoso, Isabel, additional, Bernal, Juan A., additional, and Jalife, José, additional

Published
2021
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105. Transcriptome and proteome mapping in the sheep atria reveal molecular featurets of atrial fibrillation progression

Author

Agencia Estatal de Investigación (España), Fondation Leducq, University of Michigan, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Álvarez-Franco, Alba, Rouco, Raquel, Ramírez, Rafael J., Guerrero-Serna, Guadalupe, Tiana, María, Cogliati, Sara, Kaur, Kuljeet, Saeed, Muhammed, Magni, Ricardo, Enríquez, José Antonio, Sánchez-Cabo, Fátima, Jalife, José, Manzanares, Miguel, Agencia Estatal de Investigación (España), Fondation Leducq, University of Michigan, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Álvarez-Franco, Alba, Rouco, Raquel, Ramírez, Rafael J., Guerrero-Serna, Guadalupe, Tiana, María, Cogliati, Sara, Kaur, Kuljeet, Saeed, Muhammed, Magni, Ricardo, Enríquez, José Antonio, Sánchez-Cabo, Fátima, Jalife, José, and Manzanares, Miguel

Abstract

Aims: Atrial fibrillation (AF) is a progressive cardiac arrhythmia that increases the risk of hospitalization and adverse cardiovascular events. There is a clear demand for more inclusive and large-scale approaches to understand the molecular drivers responsible for AF, as well as the fundamental mechanisms governing the transition from paroxysmal to persistent and permanent forms. In this study, we aimed to create a molecular map of AF and find the distinct molecular programmes underlying cell type-specific atrial remodelling and AF progression. Methods and results: We used a sheep model of long-standing, tachypacing-induced AF, sampled right and left atrial tissue, and isolated cardiomyocytes (CMs) from control, intermediate (transition), and late time points during AF progression, and performed transcriptomic and proteome profiling. We have merged all these layers of information into a meaningful three-component space in which we explored the genes and proteins detected and their common patterns of expression. Our data-driven analysis points at extracellular matrix remodelling, inflammation, ion channel, myofibril structure, mitochondrial complexes, chromatin remodelling, and genes related to neural function, as well as critical regulators of cell proliferation as hallmarks of AF progression. Most important, we prove that these changes occur at early transitional stages of the disease, but not at later stages, and that the left atrium undergoes significantly more profound changes than the right atrium in its expression programme. The pattern of dynamic changes in gene and protein expression replicate the electrical and structural remodelling demonstrated previously in the sheep and in humans, and uncover novel mechanisms potentially relevant for disease treatment. Conclusions: Transcriptomic and proteomic analysis of AF progression in a large animal model shows that significant changes occur at early stages, and that among others involve previously undescribed in

Published
2021

106. Datasets related to a study aimed to identify genetic markers of CDA by subphenotypes associated with cardiotoxicity

Author

European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Junta de Castilla y León, Fundación la Caixa, Centro Nacional de Investigaciones Cardiovasculares (España), Pérez-Losada, J. [0000-0003-2400-624X], Macías de Plasencia, Guillermo, Fraile, Susana, Rodrigues Teixeira, Telmo, Hernández-García, María Ángeles, Holgado-Madruga, M., González-Neira, Ana, Sánchez, Pedro L., Pérez-Losada, J., Gómez-Vecino, Aurora, Corchado Cobos, Roberto, Blanco-Gómez, Adrián, Castillo, Sonia, García-Sancha, Natalia, Martin-Garcia, Ana, Prieto, Carlos, Ruiz-Pinto, Sara, Pita, Guillermo, Velasco-Ruiz, Alejandro, Patino-Alonso, María Carmen, Galindo-Villardón, Purificación, Linarejos Vera-Pedrosa, María, Jalife, José, Castellanos-Martín, Andrés, Sáez-Freire, María del Mar, Mendiburu-Eliçabe, Marina, García-Macías, Carmen, Galvis-Jiménez, Julie Milena, García-Sánchez, Asunción, Isidoro-García, María, Fuentes, Manuel, García-Cenador, Begoña, García-Criado, Francisco Javier, García, Juan L., Cruz, Juan Jesús, Rodríguez-Sánchez, César Augusto, Martín-Ruiz, Alejandro, Pérez-López, Estefanía, Pérez-Martínez, Antonio, Gutiérrez-Larraya, Federico, Cartón, Antonio J., García-Saenz, José Ángel, Patiño-García, Ana, Martin, Miguel, Alonso Gordoa, Teresa, Vulsteke, Christof, Croes, Lieselot, Hatse, Sigrid, Van Brussel, Thomas, Lambrechts, Diether, Wildiers, Hans, Martín, Miguel A., European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Junta de Castilla y León, Fundación la Caixa, Centro Nacional de Investigaciones Cardiovasculares (España), Pérez-Losada, J. [0000-0003-2400-624X], Macías de Plasencia, Guillermo, Fraile, Susana, Rodrigues Teixeira, Telmo, Hernández-García, María Ángeles, Holgado-Madruga, M., González-Neira, Ana, Sánchez, Pedro L., Pérez-Losada, J., Gómez-Vecino, Aurora, Corchado Cobos, Roberto, Blanco-Gómez, Adrián, Castillo, Sonia, García-Sancha, Natalia, Martin-Garcia, Ana, Prieto, Carlos, Ruiz-Pinto, Sara, Pita, Guillermo, Velasco-Ruiz, Alejandro, Patino-Alonso, María Carmen, Galindo-Villardón, Purificación, Linarejos Vera-Pedrosa, María, Jalife, José, Castellanos-Martín, Andrés, Sáez-Freire, María del Mar, Mendiburu-Eliçabe, Marina, García-Macías, Carmen, Galvis-Jiménez, Julie Milena, García-Sánchez, Asunción, Isidoro-García, María, Fuentes, Manuel, García-Cenador, Begoña, García-Criado, Francisco Javier, García, Juan L., Cruz, Juan Jesús, Rodríguez-Sánchez, César Augusto, Martín-Ruiz, Alejandro, Pérez-López, Estefanía, Pérez-Martínez, Antonio, Gutiérrez-Larraya, Federico, Cartón, Antonio J., García-Saenz, José Ángel, Patiño-García, Ana, Martin, Miguel, Alonso Gordoa, Teresa, Vulsteke, Christof, Croes, Lieselot, Hatse, Sigrid, Van Brussel, Thomas, Lambrechts, Diether, Wildiers, Hans, and Martín, Miguel A.

Abstract

Here we present a series of supplemental datasets that complement our study entitled "A Systems Genetics approach to identify genetic markers of cardiotoxicity due to anthracyclines in cancer patients." The datasets presented here were used to generate the main and supplementary figures and tables of the indicated study. The study consists of the identification of genetic markers of cardiotoxicity due to anthracyclines (CDA). CDA is a complex genesis disease or complex trait, and because of this, there is a component of missing heritability. Therefore, it is not possible to identify genetic markers associated with CDA risk. Here, we propose that molecular subphenotypes associated with the CDA may be a strategy for identifying some of this missing heritability and risk markers associated with it. A similar strategy could be applied to identify markers of other diseases of complex genesis. This study is done using a genetically heterogeneous cohort of mice that developed breast cancer and was treated with doxorubicin or a combined treatment of doxorubicin and docetaxel. The mouse cohort was generated by backcrossing, so each mouse is genetically unique. Post-chemotherapy heart damage was assessed by quantifying fibrosis's cardiac area and the thickness of myocardial fibers. The genetic regions associated with CDA were assessed by massive genotyping and genetic linkage analysis. Several molecular subphenotypes were quantified in the myocardium, and their association with the CDA was evaluated. Subsequently, we identified which of them were most statistically associated with CDA in multivariate models. Moreover, which complex trait loci (QTLs) associated with molecular subphenotypes best explained CDA. This strategy served to identify in the cohort of mice genes whose allelic forms could be candidates for the risk of CDA. Allelic variants of these genes were evaluated in four cohorts of cancer patients treated with anthracyclines and whose CDA was evaluated by echocardi

Published
2021

115. Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson–Gilford progeria syndrome

Author

Macías, Álvaro, primary, Díaz-Larrosa, J Jaime, additional, Blanco, Yaazan, additional, Fanjul, Víctor, additional, González-Gómez, Cristina, additional, Gonzalo, Pilar, additional, Andrés-Manzano, María Jesús, additional, da Rocha, Andre Monteiro, additional, Ponce-Balbuena, Daniela, additional, Allan, Andrew, additional, Filgueiras-Rama, David, additional, Jalife, José, additional, and Andrés, Vicente, additional

Published
2021
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121. Contributors

Author

Abdula, Raushan, primary, Ackerman, Michael J., additional, Akhtar, Masood, additional, Anand, Rishi, additional, Anderson, Kelley, additional, Antzelevitch, Charles, additional, Auricchio, Angelo, additional, Badhwar, Nitish, additional, Bailey, Shane, additional, Barrett, Conor D., additional, de Luna, Antonio Bayes, additional, Belk, Paul, additional, Benditt, David G., additional, Benito, Begoña, additional, Bennett, Matthew T., additional, Bharati, Saroja, additional, Bharucha, David B., additional, Bonney, William J., additional, Bowles, Neil E., additional, Boyden, Penelope A., additional, Bozorgnia, Babak, additional, Breithardt, Günter, additional, Brugada, Josep, additional, Brugada, Pedro, additional, Brugada, Ramon, additional, Burkart, Thomas Adam, additional, Burkhardt, J. David, additional, Calkins, Hugh, additional, Camm, A. John, additional, Cecchi, Franco, additional, Cerrone, Marina, additional, Chattipakorn, Nipon, additional, Chen, Shih-Ann, additional, Chicos, Alexandru B., additional, Choudhuri, Indrajit, additional, Clauss, Sebastien, additional, Conti, Jamie Beth, additional, Cordeiro, Jonathan M., additional, Cuneo, Bettina F., additional, Cunha, Shane R., additional, Curtis, Anne B., additional, Cutler, Michael J., additional, Cygankiewicz, Iwona, additional, Damiano, Ralph J., additional, Daubert, James P., additional, Daubert, Jean-Claude, additional, Davies, D. Wyn, additional, Deedwania, Prakash, additional, DeGroot, Paul J., additional, Derval, Nicolas, additional, Biase, Luigi Di, additional, Dickfeld, Timm-Michael, additional, Dobrev, Dobromir, additional, Domanski, Michael, additional, Dorian, Paul, additional, Doshi, Hiten, additional, Duffy, Heather S., additional, Eckardt, Lars, additional, Eisner, David, additional, Ellenbogen, Kenneth A., additional, Elliott, Perry M., additional, El-Sherif, Nabil, additional, Ernst, Sabine, additional, Estes, N.A. Mark, additional, Ezekowitz, Michael D., additional, Fisher, John D., additional, Fishman, Glenn I., additional, Forclaz, Andrei, additional, Gallinghouse, G. Joseph, additional, Garlitski, Ann C., additional, Gerstenfeld, Edward P., additional, Gill, Jaswinder, additional, Gillis, Anne M., additional, Goebel, Jason A., additional, Gold, Michael R., additional, Goldman, Pamela S.N., additional, Goldschlager, Nora, additional, Gula, Lorne J., additional, Haïssaguerre, Michel, additional, Hamel, John-John, additional, Hegland, Donald D., additional, Hettrick, Douglas, additional, Ho, Siew Yen, additional, Hocini, Mélèze, additional, Homoud, Munther K., additional, Horton, Rodney, additional, Huizar, Jose F., additional, Hund, Thomas J., additional, Ideker, Raymond E., additional, Iyer, Ramesh, additional, Jackson, Kevin P., additional, Jadidi, Amir, additional, Jaïs, Pierre, additional, Jalife, José, additional, Janse, Michiel, additional, Jordaens, Luc, additional, Jung, Werner, additional, Kääb, Stefan, additional, Kadish, Alan H., additional, Kalman, Jonathan M., additional, Kantharia, Bharat K., additional, Kaszala, Karoly, additional, Katritsis, Demosthenes G., additional, Kaufman, Elizabeth S., additional, Kim, Susan S., additional, Kirubakaran, Senthil, additional, Klein, George J., additional, Klein, Helmut, additional, Knecht, Sébastien, additional, Knight, Bradley, additional, Knops, Paul, additional, Koruth, Jacob S., additional, Kowey, Peter R., additional, Krahn, Andrew D., additional, Krumerman, Andrew, additional, Kuriachan, Vikas, additional, Kusumoto, Fred, additional, Lardizabal, Joel A., additional, Lau, Chu-Pak, additional, Lau, David H., additional, Lazzara, Ralph, additional, Lee, Anson M., additional, Leong-Sit, Peter, additional, Levy, Samuel, additional, Lewalter, Thorsten, additional, Li, Hua, additional, Lindsay, Bruce D., additional, Linton, Nick W.F., additional, Madan, Nandini, additional, Mahomed, Yousuf, additional, Malcolme-Lawes, Louisa, additional, Marchlinski, Frank, additional, Maron, Barry J., additional, McBride, Ruth, additional, McKenna, William J., additional, Mehra, Rahul, additional, Mehta, Anjlee M., additional, Miller, John M., additional, Mitchell, L. Brent, additional, Mohler, Peter J., additional, Morillo, Carlos A., additional, Muir, Alison R., additional, Myazaki, Shisuke, additional, Myerburg, Robert J., additional, Naccarelli, Gerald V., additional, Nagarakanti, Rangadham, additional, Nanda, Navin C., additional, Napolitano, Carlo, additional, Natale, Andrea, additional, Nattel, Stanley, additional, Nault, Isabelle, additional, Noujaim, Sami F., additional, Olivotto, Iacopo, additional, Omran, Heyder, additional, Padeletti, Luigi, additional, Page, Richard L., additional, Park, David S., additional, Preminger, Mark, additional, Priori, Silvia G., additional, Quan, Kara J., additional, Raj, Satish R., additional, Rawlins, John, additional, Razak, Shakeeb, additional, Reddy, Shantanu, additional, Reddy, Vivek Y., additional, Rho, Robert W., additional, Rhodes, Larry A., additional, Rivero, Abel, additional, Robinson, Melissa, additional, Robotis, Dionyssios, additional, Roden, Dan M., additional, Root, Michael J., additional, Rosen, Michael R., additional, Rosenbaum, David, additional, Ruskin, Jeremy, additional, Sacher, Frédéric, additional, Sakaguchi, Scott, additional, Saksena, Sanjeev, additional, Sanchez, Javier, additional, Santageli, Pasquale, additional, Savelieva, Irina, additional, Schoenfeld, Mark H., additional, Schwartz, Peter J., additional, Schweikert, Robert, additional, Segal, Oliver R., additional, Shah, Dipen, additional, Shah, Maully, additional, Sharma, Arjun, additional, Sharma, Sanjay, additional, Sheldon, Robert S., additional, Shinagawa, Kaori, additional, Singh, Bramah N., additional, Singh, Steven, additional, Siu, Chung-Wah, additional, Skadsberg, Nicholas D., additional, Skanes, Allan C., additional, Slee, April, additional, Sra, Jasbir, additional, Steinbeck, Gerhard, additional, Steinhaus, David, additional, Stevenson, William G., additional, Strasburger, Janette F., additional, Sy, Raymond W., additional, Teh, Andrew W., additional, Tester, David J., additional, Tomaselli, Gordon, additional, Towbin, Jeffrey A., additional, Turgeon, Jacques, additional, Turitto, Gioia, additional, Tzou, Wendy, additional, van Dijk, J. Gert, additional, Van Hare, George F., additional, Van Houzen, Nathan, additional, Vatta, Matteo, additional, Vedantham, Vasanth, additional, Vetter, Victoria L., additional, Voeller, Rochus K., additional, Wagner, Galen, additional, Wakili, Reza, additional, Walker, Mariah L., additional, Wang, Paul J., additional, Wit, Andrew L., additional, Wright, Matthew, additional, Yee, Raymond, additional, Zagrodsky, Jason D., additional, Zareba, Wojciech, additional, Zellerhoff, Stephan, additional, and Ziegler, Paul, additional

Published
2012
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125. Tbx5 variants disrupt Nav1.5 function differently in patients diagnosed with Brugada or Long QT Syndrome.

Author

Nieto-Marín, Paloma, Tinaquero, David, Utrilla, Raquel G, Cebrián, Jorge, González-Guerra, Andrés, Crespo-García, Teresa, Cámara-Checa, Anabel, Rubio-Alarcón, Marcos, Dago, María, Alfayate, Silvia, Filgueiras-Rama, David, Peinado, Rafael, López-Sendón, José Luis, Jalife, José, Tamargo, Juan, Bernal, Juan Antonio, Caballero, Ricardo, Delpón, Eva, and Investigators, the ITACA Consortium

Subjects
LONG QT syndrome, ARRHYTHMIA, ACTION potentials, BRUGADA syndrome, MUTANT proteins, TRANSCRIPTION factors
Abstract

Aims The transcription factor Tbx5 controls cardiogenesis and drives Scn5a expression in mice. We have identified two variants in TBX5 encoding p. D111Y and p. F206L Tbx5, respectively, in two unrelated patients with structurally normal hearts diagnosed with long QT (LQTS) and Brugada (BrS) syndrome. Here, we characterized the consequences of each variant to unravel the underlying disease mechanisms. Methods and results We combined clinical analysis with in vivo and in vitro electrophysiological and molecular techniques in human-induced pluripotent stem-cell-derived cardiomyocytes (hiPSC-CMs), HL-1 cells, and cardiomyocytes from mice trans -expressing human wild-type (WT) or mutant proteins. Tbx5 increased transcription of SCN5A encoding cardiac Nav1.5 channels, while repressing CAMK2D and SPTBN4 genes encoding Ca/calmodulin kinase IIδ (CaMKIIδ) and βIV-spectrin, respectively. These effects significantly increased Na current (INa) in hiPSC-CMs and in cardiomyocytes from mice trans -expressing Tbx5. Consequently, action potential (AP) amplitudes increased and QRS interval narrowed in the mouse electrocardiogram. p. F206L Tbx5 bound to the SCN5A promoter failed to transactivate it, thus precluding the pro-transcriptional effect of WT Tbx5. Therefore, p. F206L markedly decreased INa in hiPSC-CM, HL-1 cells and mouse cardiomyocytes. The INa decrease in p. F206L trans -expressing mice translated into QRS widening and increased flecainide sensitivity. p. D111Y Tbx5 increased SCN5A expression but failed to repress CAMK2D and SPTBN4. The increased CaMKIIδ and βIV-spectrin significantly augmented the late component of INa (INaL) which, in turn, significantly prolonged AP duration in both hiPSC-CMs and mouse cardiomyocytes. Ranolazine, a selective INaL inhibitor, eliminated the QT and QTc intervals prolongation seen in p. D111Y trans -expressing mice. Conclusions In addition to peak INa, Tbx5 critically regulates INaL and the duration of repolarization in human cardiomyocytes. Our original results suggest that TBX5 variants associate with and modulate the intensity of the electrical phenotype in LQTS and BrS patients. [ABSTRACT FROM AUTHOR]

Published
2022
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128. Venice Chart International Consensus Document on Atrial Fibrillation Ablation: 2011 Update

Author

RAVIELE, ANTONIO, NATALE, ANDREA, CALKINS, HUGH, CAMM, JOHN A., CAPPATO, RICCARDO, ANN CHEN, SHIH, CONNOLLY, STUART J., DAMIANO JR, RALPH, DE PONTI, ROBERTO, EDGERTON, JAMES R., HAÏSSAGUERRE, MICHEL, HINDRICKS, GERHARD, HO, SIEW Y., JALIFE, JOSÉ, KIRCHHOF, PAULUS, KOTTKAMP, HANS, KUCK, KARL H., MARCHLINSKI, FRANCIS E., PACKER, DOUGLAS L., PAPPONE, CARLO, PRYSTOWSKY, ERIC, REDDY, VIVEK K., THEMISTOCLAKIS, SAKIS, VERMA, ATUL, WILBER, DAVID J., and WILLEMS, STEPHAN

Published
2012
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129. 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design: A report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Developed in partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Society (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bodies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Society, and the Heart Rhythm Society

Author

Calkins, Hugh, Kuck, Karl Heinz, Cappato, Riccardo, Brugada, Josep, Camm, A. John, Chen, Shih-Ann, Crijns, Harry J.G., Damiano, Ralph J., Jr., Davies, D. Wyn, DiMarco, John, Edgerton, James, Ellenbogen, Kenneth, Ezekowitz, Michael D., Haines, David E., Haissaguerre, Michel, Hindricks, Gerhard, Iesaka, Yoshito, Jackman, Warren, Jalife, Jose, Jais, Pierre, Kalman, Jonathan, Keane, David, Kim, Young-Hoon, Kirchhof, Paulus, Klein, George, Kottkamp, Hans, Kumagai, Koichiro, Lindsay, Bruce D., Mansour, Moussa, Marchlinski, Francis E., McCarthy, Patrick M., Mont, J. Lluis, Morady, Fred, Nademanee, Koonlawee, Nakagawa, Hiroshi, Natale, Andrea, Nattel, Stanley, Packer, Douglas L., Pappone, Carlo, Prystowsky, Eric, Raviele, Antonio, Reddy, Vivek, Ruskin, Jeremy N., Shemin, Richard J., Tsao, Hsuan-Ming, Wilber, David, Calkins, Hugh, Kuck, Karl Heinz, Cappato, Riccardo, Chen, Shih-Ann, Prystowsky, Eric N., Kuck, Karl Heinz, Natale, Andrea, Haines, David E., Marchlinski, Francis E., Calkins, Hugh, Davies, D. Wyn, Lindsay, Bruce D., Damiano, Ralph, Jr., Packer, Douglas L., Brugada, Josep, Camm, A. John, Crijns, Harry J.G., DiMarco, John, Edgerton, James, Ellenbogen, Kenneth, Ezekowitz, Michael D., Haissaguerre, Michel, Hindricks, Gerhard, Iesaka, Yoshito, Jackman, Warren M., Jais, Pierre, Jalife, José, Kalman, Jonathan, Keane, David, Kim, Young-Hoon, Kirchhof, Paulus, Klein, George, Kottkamp, Hans, Kumagai, Koichiro, Mansour, Moussa, Marchlinski, Francis, McCarthy, Patrick, Mont, J. Lluis, Morady, Fred, Nademanee, Koonlawee, Nakagawa, Hiroshi, Nattel, Stanley, Pappone, Carlo, Raviele, Antonio, Reddy, Vivek, Ruskin, Jeremy N., Shemin, Richard J., Tsao, Hsuan-Ming, Wilber, David, Ad, Niv, Cummings, Jennifer, Gillinov, A. Mark, Heidbuchel, Hein, January, Craig, Lip, Gregory, Markowitz, Steven, Nair, Mohan, Ovsyshcher, I. Eli, Pak, Hui-Nam, Tsuchiya, Takeshi, Shah, Dipen, Siong, Teo Wee, and Vardas, Panos E.

Published
2012
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136. Transcriptome and proteome mapping in the sheep atria reveal molecular featurets of atrial fibrillation progression

Author

Alvarez-Franco, Alba, primary, Rouco, Raquel, additional, Ramirez, Rafael J, additional, Guerrero-Serna, Guadalupe, additional, Tiana, Maria, additional, Cogliati, Sara, additional, Kaur, Kuljeet, additional, Saeed, Mohammed, additional, Magni, Ricardo, additional, Enriquez, Jose Antonio, additional, Sanchez-Cabo, Fatima, additional, Jalife, José, additional, and Manzanares, Miguel, additional

Published
2020
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137. Kir2.1 Interactome Mapping Uncovers PKP4 as a Modulator of the Kir2.1-Regulated Inward Rectifier Potassium Currents

Author

Park, Sung-Soo, primary, Ponce-Balbuena, Daniela, additional, Kuick, Rork, additional, Guerrero-Serna, Guadalupe, additional, Yoon, Justin, additional, Mellacheruvu, Dattatreya, additional, Conlon, Kevin P., additional, Basrur, Venkatesha, additional, Nesvizhskii, Alexey I., additional, Jalife, José, additional, and Rual, Jean-François, additional

Published
2020
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138. Personalized monitoring of electrical remodelling during atrial fibrillation progression via remote transmissions from implantable devices

Author

Lillo-Castellano, José María, primary, González-Ferrer, Juan José, primary, Marina-Breysse, Manuel, primary, Martínez-Ferrer, José Bautista, primary, Pérez-Álvarez, Luisa, primary, Alzueta, Javier, primary, Martínez, Juan Gabriel, primary, Rodríguez, Aníbal, primary, Rodríguez-Pérez, Juan Carlos, primary, Anguera, Ignasi, primary, Viñolas, Xavier, primary, García-Alberola, Arcadio, primary, Quintanilla, Jorge G, primary, Alfonso-Almazán, José Manuel, primary, García, Javier, primary, Borrego, Luis, primary, Cañadas-Godoy, Victoria, primary, Pérez-Castellano, Nicasio, primary, Pérez-Villacastín, Julián, primary, Jiménez-Díaz, Javier, primary, Jalife, José, primary, and Filgueiras-Rama, David, primary

Published
2019
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141. Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson–Gilford progeria syndrome.

Author

Macías, Álvaro, Díaz-Larrosa, J Jaime, Blanco, Yaazan, Fanjul, Víctor, González-Gómez, Cristina, Gonzalo, Pilar, Andrés-Manzano, María Jesús, Rocha, Andre Monteiro da, Ponce-Balbuena, Daniela, Allan, Andrew, Filgueiras-Rama, David, Jalife, José, and Andrés, Vicente

Subjects
HEART conduction system, PROGERIA, PACLITAXEL, HEART beat, LABORATORY mice
Abstract

Aims Hutchinson–Gilford progeria syndrome (HGPS) is an ultrarare laminopathy caused by expression of progerin, a lamin A variant, also present at low levels in non-HGPS individuals. HGPS patients age and die prematurely, predominantly from cardiovascular complications. Progerin-induced cardiac repolarization defects have been described previously, although the underlying mechanisms are unknown. Methods and results We conducted studies in heart tissue from progerin-expressing LmnaG609G/G609G (G609G) mice, including microscopy, intracellular calcium dynamics, patch-clamping, in vivo magnetic resonance imaging, and electrocardiography. G609G mouse cardiomyocytes showed tubulin-cytoskeleton disorganization, t-tubular system disruption, sarcomere shortening, altered excitation–contraction coupling, and reductions in ventricular thickening and cardiac index. G609G mice exhibited severe bradycardia, and significant alterations of atrio-ventricular conduction and repolarization. Most importantly, 50% of G609G mice had altered heart rate variability, and sinoatrial block, both significant signs of premature cardiac aging. G609G cardiomyocytes had electrophysiological alterations, which resulted in an elevated action potential plateau and early afterdepolarization bursting, reflecting slower sodium current inactivation and long Ca+2 transient duration, which may also help explain the mild QT prolongation in some HGPS patients. Chronic treatment with low-dose paclitaxel ameliorated structural and functional alterations in G609G hearts. Conclusions Our results demonstrate that tubulin-cytoskeleton disorganization in progerin-expressing cardiomyocytes causes structural, cardiac conduction, and excitation–contraction coupling defects, all of which can be partially corrected by chronic treatment with low dose paclitaxel. [ABSTRACT FROM AUTHOR]

Published
2022
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144. Contributors

Author

ACKERMAN, MICHAEL J., primary, AGUEL, FELIPE, additional, ALBERTE-LISTA, CESAR, additional, ANTZ, MATTHIAS, additional, ANTZELEVITCH, CHARLES, additional, ANUMONWO, JUSTUS M.B., additional, ARORA, RISHI, additional, BACKX, PETER H., additional, BALSER, JEFFREY R., additional, BECKMAN, KAREN, additional, BENDITT, DAVID G., additional, BERBARI, EDWARD J., additional, BERENFELD, OMER, additional, BERS, DONALD M., additional, BEYER, ERIC C., additional, BIEL, MARTIN, additional, BOWLES, NEIL E., additional, BOYETT, MARK R., additional, BRUGADA, JOSEP, additional, BRUGADA, PEDRO, additional, BRUGADA, RAMON, additional, BURSAC, NENAD, additional, BUXTON, ALFRED E., additional, CAIN, MICHAEL E., additional, CALKINS, HUGH, additional, CALLANS, DAVID J., additional, CAPPATO, RICCARDO, additional, CARROLL, SHEILA J., additional, CASTELLANOS, AGUSTIN, additional, CHEN, LAN S., additional, CHEN, PENG-SHENG, additional, CHEN, SHIN-ANN, additional, CHEN, XIONGWEN, additional, CLAPHAM, DAVID E., additional, CLÉMENTY, JACQUES, additional, CRIJNS, HARRY J., additional, DAOUD, EMILE G., additional, DAS, MITHILESH K., additional, DELMAR, MARIO, additional, DIFRANCESCO, DARIO, additional, DIMARCO, JOHN P., additional, DOBRZYNSKI, HALINA, additional, DUFFY, HEATHER S., additional, EFIMOV, IGOR R., additional, EHRLICH, JOACHIM R., additional, EL-SHERIF, NABIL, additional, ELLENBOGEN, KENNETH A., additional, EPSTEIN, ANDREW E., additional, ERMIS, CENGIZ, additional, ERNST, SABINE, additional, ESTES, N. A. MARK, additional, FAST, VLADIMIR G., additional, FEDOROV, VADIM V., additional, FONTAINE, GUY, additional, FORESTI, SARA, additional, FORNES, PAUL, additional, FRANK, ROBERT, additional, FRANZ, MICHAEL R., additional, GALVIN, JOSEPH M., additional, GARFINKEL, ALAN, additional, GILLIS, ANNE M., additional, GOLD, MICHAEL R., additional, GOLDBERGER, JEFFREY, additional, GRAY, RICHARD A., additional, GRIMM, WOLFRAM, additional, GROH, WILLIAM J., additional, HAINES, DAVID E., additional, HAÏSSAGUERRE, MICHEL, additional, HARO, CARLOS, additional, HAYES, DAVID L., additional, HAYRAPETYAN, VOLODYA, additional, HEBERT, JEAN-LOUIS, additional, HENRIQUEZ, CRAIG S., additional, HERRMANN, STEFAN, additional, HINDRICKS, GERHARD, additional, HOCINI, MÉLÈZE, additional, HOFMANN, FRANZ, additional, HOHNLOSER, STEFAN H., additional, HONJO, HARUO, additional, HOUSER, STEVEN R., additional, HRYSHKO, LARRY V., additional, HSU, EDWARD W., additional, HUANG, JIAN, additional, HULOT, JEAN-SÉBASTIEN, additional, HUTCHINS, GARY D., additional, IDEKER, RAYMOND E., additional, INTERIAN, ALBERTO, additional, IWAI, SEI, additional, JACKMAN, WARREN M., additional, JAÏS, PIERRE, additional, JALIFE, JOSÉ, additional, JANUARY, CRAIG T., additional, JOHNSON, CHRISTOPHER R., additional, JOSEPHSON, MARK E., additional, JOUVEN, XAVIER, additional, KADISH, ALAN H., additional, KALMAN, JONATHAN M., additional, KAMP, TIMOTHY J., additional, KASS, ROBERT S., additional, KENNEDY, HAROLD L., additional, KERBER, RICHARD E., additional, KHOSITSETH, ANANT, additional, KILBORN, MICHAEL J., additional, KLÉBER, ANDRÉ G., additional, KLEIN, GEORGE J., additional, KNIGHT, BRADLEY P., additional, KODAMA, ITSUO, additional, KOTTKAMP, HANS, additional, KRAHN, ANDREW D., additional, KUCERA, JAN P., additional, KUCK, KARL-HEINZ, additional, KUGLER, JOHN D., additional, KUO, CHI TAI, additional, KUROKAWA, JUNKO, additional, LAB, MAX J., additional, LAI, WEN TER, additional, LARSON, CLAIRE, additional, LAURITA, KENNETH R., additional, LAZZARA, RALPH, additional, LERMAN, BRUCE B., additional, LERNER, DEBORAH L., additional, LÉVY, SAMUEL, additional, LI, RONALD A., additional, LIN, DAVID, additional, LOCKWOOD, DEBORAH, additional, LONDON, BARRY, additional, LÜ, FEI, additional, LUDWIG, ANDREAS, additional, MAKIELSKI, JONATHAN C., additional, MALIK, MAREK, additional, MARBÁN, EDUARDO, additional, MARCHLINSKI, FRANCIS E., additional, MARKIDES, VIAS, additional, MARKOWITZ, STEVEN M., additional, MARON, BARRY J., additional, MARTÍNEZ, AGUSTÍN D., additional, MCGUIRE, MARK A., additional, MEISSNER, GERHARD, additional, MILES, WILLIAM M., additional, MILLER, JOHN M., additional, MILLER, MICHAEL A., additional, MITTAL, SUNEET, additional, MOLEIRO, FEDERICO, additional, MOOSMANG, SVEN, additional, MORADY, FRED, additional, MORENO, ALONSO P., additional, MOSS, ARTHUR J., additional, MYERBURG, ROBERT J., additional, NAKAGAWA, HIROSHI, additional, NAPOLITANO, CARLO, additional, NATTEL, STANLEY, additional, NERBONNE, JEANNE M., additional, NIKOLSKI, VLADIMIR P., additional, OLGIN, JEFFREY E., additional, ORAL, HAKAN, additional, OTOMO, KENICHIRO, additional, OUDIT, GAVIN Y., additional, OUYANG, FEIFAN, additional, PAGÉ, PIERRE L., additional, PAPPONE, CARLO, additional, PATTERSON, EUGENE, additional, PERTSOV, ARKADY M., additional, PETERS, NICHOLAS S., additional, PETERS, ROBERT W., additional, PRIORI, SILVIA G., additional, PROST-SQUARCIONI, CATHERINE, additional, PRYSTOWSKI, ERIC N., additional, PUNSKE, BONNIE B., additional, QU, ZHILIN, additional, RAMIREZ, RAFAEL J., additional, RIVOLTA, ILARIA, additional, ROBINSON, RICHARD B., additional, RODEN, DAN M., additional, ROHR, STEPHAN, additional, ROSANIO, SALVATORE, additional, ROSEN, MICHAEL R., additional, ROSENBAUM, DAVID S., additional, ROSENSHTRAUKH, LEONID V., additional, ROTH, BRADLEY J., additional, RUDY, YORAM, additional, RUSKIN, JEREMY N., additional, SACHS, FREDERICK, additional, SAFFITZ, JEFFREY E., additional, SANDERS, PRASHANTHAN, additional, SANGUINETTI, MICHAEL C., additional, SAOUDI, NADIR, additional, SCHERLAG, BENJAMIN J., additional, SCHWARTZ, PETER J., additional, SCHWARTZMAN, DAVID, additional, SEGAL, OLIVER R., additional, SHAH, DIPEN C., additional, SHARIFOV, OLEG F., additional, SHIVKUMAR, KALYANAM, additional, SIMMONS, JEFFREY, additional, SINGH, BRAMAH N., additional, SKANES, ALLAN C., additional, SMITH, TIMOTHY W., additional, SOEJIMA, KYOKO, additional, SORGEN, PAUL L., additional, SPRAY, DAVID C., additional, SRINIVAS, MIDUTURU, additional, STEIN, KENNETH M., additional, STEINBERG, SUSAN F., additional, STEVENSON, WILLIAM G., additional, STIEBER, JULIANE, additional, STRAMBA-BADIALE, MARCO, additional, STRICKBERGER, S. ADAM, additional, SUNG, RUEY J., additional, SWEENEY, MICHAEL O., additional, SWERDLOW, CHARLES D., additional, TACCARDI, BRUNO, additional, TAFFET, STEVEN M., additional, TAI, CHING-TAI, additional, THOMAS, DANIEL, additional, TOMASELLI, GORDON F., additional, TONDATO, FERNANDO, additional, TOWBIN, JEFFREY A., additional, TRANQUILLO, JOSEPH V., additional, TRAYANOVA, NATALIA A., additional, TRIEDMAN, JOHN K., additional, TRISTANI-FIROUZI, MARTIN, additional, TSAI, CHIN-FENG, additional, TUNG, LESLIE, additional, TURITTO, GIOIA, additional, VAN HARE, GEORGE F., additional, VAN WAGONER, DAVID R., additional, VOS, MARC A., additional, WALCOTT, GREGORY P., additional, WALDO, ALBERT L., additional, WANG, ZULU, additional, WEINBERG, KENNETH M., additional, WEINSTEIN, DAVID, additional, WELLNER, MARCEL, additional, WILKOFF, BRUCE L., additional, WOOD, MARK A., additional, WU, JIANYI, additional, WU, JIASHIN, additional, WYSE, D. GEORGE, additional, YAMADA, KATHRYN A., additional, YE, BIN, additional, YEE, RAYMOND, additional, ZAITSEV, ALEXEY V., additional, ZAREBA, WOJCIECH, additional, ZHONG, GUOQIANG, additional, and ZIPES, DOUGLAS P., additional

Published
2004
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