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1. Intermediate Molecular Phenotypes to Identify Genetic Markers of Anthracycline-Induced Cardiotoxicity Risk.

Author

Gómez-Vecino, Aurora, Corchado-Cobos, Roberto, Blanco-Gómez, Adrián, García-Sancha, Natalia, Castillo-Lluva, Sonia, Martín-García, Ana, Mendiburu-Eliçabe, Marina, Prieto, Carlos, Ruiz-Pinto, Sara, Pita, Guillermo, Velasco-Ruiz, Alejandro, Patino-Alonso, Carmen, Galindo-Villardón, Purificación, Vera-Pedrosa, María, Jalife, José, Macías de Plasencia, Guillermo, Castellanos-Martín, Andrés, Sáez-Freire, María, Fraile-Martín, Susana, Rodrigues-Teixeira, Telmo, García-Macías, Carmen, Galvis-Jiménez, Julie, García-Sánchez, Asunción, Isidoro-García, María, Fuentes, Manuel, García-Cenador, María, García-Criado, Francisco, García-Hernández, Juan, Hernández-García, María, Cruz-Hernández, Juan, Rodríguez-Sánchez, César, García-Sancho, Alejandro, Pérez-López, Estefanía, Pérez-Martínez, Antonio, Gutiérrez-Larraya, Federico, Cartón, Antonio, García-Sáenz, José, Patiño-García, Ana, Martín, Miguel, Alonso-Gordoa, Teresa, Vulsteke, Christof, Croes, Lieselot, Hatse, Sigrid, Van Brussel, Thomas, Lambrechts, Diether, Wildiers, Hans, Chang, Hang, Holgado-Madruga, Marina, González-Neira, Anna, Sánchez, Pedro, Pérez Losada, Jesús, and Mao, Jian-Hua

Subjects
anthracyclines, cardiotoxicity, complex genetic disease, intermediate molecular phenotypes, quantitative trait loci, Female, Animals, Mice, Cardiotoxicity, Anthracyclines, Genetic Markers, Antibiotics, Antineoplastic, Neoplasms, Phenotype
Abstract

Cardiotoxicity due to anthracyclines (CDA) affects cancer patients, but we cannot predict who may suffer from this complication. CDA is a complex trait with a polygenic component that is mainly unidentified. We propose that levels of intermediate molecular phenotypes (IMPs) in the myocardium associated with histopathological damage could explain CDA susceptibility, so variants of genes encoding these IMPs could identify patients susceptible to this complication. Thus, a genetically heterogeneous cohort of mice (n = 165) generated by backcrossing were treated with doxorubicin and docetaxel. We quantified heart fibrosis using an Ariol slide scanner and intramyocardial levels of IMPs using multiplex bead arrays and QPCR. We identified quantitative trait loci linked to IMPs (ipQTLs) and cdaQTLs via linkage analysis. In three cancer patient cohorts, CDA was quantified using echocardiography or Cardiac Magnetic Resonance. CDA behaves as a complex trait in the mouse cohort. IMP levels in the myocardium were associated with CDA. ipQTLs integrated into genetic models with cdaQTLs account for more CDA phenotypic variation than that explained by cda-QTLs alone. Allelic forms of genes encoding IMPs associated with CDA in mice, including AKT1, MAPK14, MAPK8, STAT3, CAS3, and TP53, are genetic determinants of CDA in patients. Two genetic risk scores for pediatric patients (n = 71) and women with breast cancer (n = 420) were generated using machine-learning Least Absolute Shrinkage and Selection Operator (LASSO) regression. Thus, IMPs associated with heart damage identify genetic markers of CDA risk, thereby allowing more personalized patient management.

Published
2023

2. p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia

Author

Romero-Becerra, Rafael, Cruz, Francisco M., Mora, Alfonso, Lopez, Juan Antonio, Ponce-Balbuena, Daniela, Allan, Andrew, Ramos-Mondragón, Roberto, González-Terán, Bárbara, León, Marta, Rodríguez, Maria Elena, Leiva-Vega, Luis, Guerrero-Serna, Guadalupe, Jimenez-Vazquez, Eric N., Filgueiras-Rama, David, Vázquez, Jesús, Jalife, José, and Sabio, Guadalupe

Published
2023
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3. Aproximación práctica para la caracterización de la miocardiopatía auricular en pacientes con fibrilación auricular

Author

La Rosa, Giulio, Morillo, Carlos A., Quintanilla, Jorge G., Doltra, Adelina, Mont, Lluis, Rodríguez-Mañero, Moisés, Sarkozy, Andrea, Merino, José Luis, Vivas, David, Datino, Tomás, Calvo, David, Pérez-Castellano, Nicasio, Pérez-Villacastín, Julián, Fauchier, Laurent, Lip, Gregory, Hatem, Stéphane N., Jalife, José, Sanchis, Laura, Marín, Francisco, and Filgueiras-Rama, David

Published
2024
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4. Practical approach for atrial cardiomyopathy characterization in patients with atrial fibrillation

Author

La Rosa, Giulio, Morillo, Carlos A., Quintanilla, Jorge G., Doltra, Adelina, Mont, Lluis, Rodríguez-Mañero, Moisés, Sarkozy, Andrea, Merino, José Luis, Vivas, David, Datino, Tomás, Calvo, David, Pérez-Castellano, Nicasio, Pérez-Villacastín, Julián, Fauchier, Laurent, Lip, Gregory, Hatem, Stéphane N., Jalife, José, Sanchis, Laura, Marín, Francisco, and Filgueiras-Rama, David

Published
2024
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7. Aproximación práctica para la caracterización de la miocardiopatía auricular en pacientes con fibrilación auricular

Author

Rosa, Giulio La, primary, Morillo, Carlos, additional, Quintanilla, Jorge G., additional, Doltra, Adelina, additional, Mont, Lluis, additional, Rodríguez-Mañero, Moisés, additional, Sarkosy, Andrea, additional, Luis Merino, José, additional, Vivas, David, additional, Datino, Tomás, additional, Calvo, David, additional, Pérez-Castellano, Nicasio, additional, Pérez-Villacastín, Julián, additional, Fauchier, Laurent, additional, Lip, Gregory, additional, Hatem, Stéphane N., additional, Jalife, José, additional, Sanchis, Laura, additional, Marín, Francisco, additional, and Filgueiras-Rama, David, additional

Published
2024
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8. Extracellular Kir2.1 C122Y Mutant Upsets Kir2.1-PIP 2 Bonds and Is Arrhythmogenic in Andersen-Tawil Syndrome

Author

Cruz, Francisco M., primary, Macías, Álvaro, additional, Moreno-Manuel, Ana I., additional, Gutiérrez, Lilian K., additional, Vera-Pedrosa, María Linarejos, additional, Martínez-Carrascoso, Isabel, additional, Sánchez Pérez, Patricia, additional, Ruiz Robles, Juan Manuel, additional, Bermúdez-Jiménez, Francisco J., additional, Díaz-Agustín, Aitor, additional, Martínez de Benito, Fernando, additional, Arias-Santiago, Salvador, additional, Braza-Boils, Aitana, additional, Martín-Martínez, Mercedes, additional, Gutierrez-Rodríguez, Marta, additional, Bernal, Juan A., additional, Zorio, Esther, additional, Jiménez-Jaimez, Juan, additional, and Jalife, José, additional

Published
2024
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9. A computational model of induced pluripotent stem‐cell derived cardiomyocytes incorporating experimental variability from multiple data sources

Author

Kernik, Divya C, Morotti, Stefano, Wu, HaoDi, Garg, Priyanka, Duff, Henry J, Kurokawa, Junko, Jalife, José, Wu, Joseph C, Grandi, Eleonora, and Clancy, Colleen E

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Heart Disease, Rare Diseases, Stem Cell Research - Induced Pluripotent Stem Cell, Bioengineering, Stem Cell Research, Genetics, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Action Potentials, Arrhythmias, Cardiac, Cardiac Conduction System Disease, Computer Simulation, Humans, Induced Pluripotent Stem Cells, Information Storage and Retrieval, Myocytes, Cardiac, Phenotype, computer modelling, iPSC-CMs, variability, Medical and Health Sciences, Physiology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Key pointsInduced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) capture patient-specific genotype-phenotype relationships, as well as cell-to-cell variability of cardiac electrical activity Computational modelling and simulation provide a high throughput approach to reconcile multiple datasets describing physiological variability, and also identify vulnerable parameter regimes We have developed a whole-cell model of iPSC-CMs, composed of single exponential voltage-dependent gating variable rate constants, parameterized to fit experimental iPSC-CM outputs We have utilized experimental data across multiple laboratories to model experimental variability and investigate subcellular phenotypic mechanisms in iPSC-CMs This framework links molecular mechanisms to cellular-level outputs by revealing unique subsets of model parameters linked to known iPSC-CM phenotypes ABSTRACT: There is a profound need to develop a strategy for predicting patient-to-patient vulnerability in the emergence of cardiac arrhythmia. A promising in vitro method to address patient-specific proclivity to cardiac disease utilizes induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). A major strength of this approach is that iPSC-CMs contain donor genetic information and therefore capture patient-specific genotype-phenotype relationships. A cited detriment of iPSC-CMs is the cell-to-cell variability observed in electrical activity. We postulated, however, that cell-to-cell variability may constitute a strength when appropriately utilized in a computational framework to build cell populations that can be employed to identify phenotypic mechanisms and pinpoint key sensitive parameters. Thus, we have exploited variation in experimental data across multiple laboratories to develop a computational framework for investigating subcellular phenotypic mechanisms. We have developed a whole-cell model of iPSC-CMs composed of simple model components comprising ion channel models with single exponential voltage-dependent gating variable rate constants, parameterized to fit experimental iPSC-CM data for all major ionic currents. By optimizing ionic current model parameters to multiple experimental datasets, we incorporate experimentally-observed variability in the ionic currents. The resulting population of cellular models predicts robust inter-subject variability in iPSC-CMs. This approach links molecular mechanisms to known cellular-level iPSC-CM phenotypes, as shown by comparing immature and mature subpopulations of models to analyse the contributing factors underlying each phenotype. In the future, the presented models can be readily expanded to include genetic mutations and pharmacological interventions for studying the mechanisms of rare events, such as arrhythmia triggers.

Published
2019

10. The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of Short QT Syndrome type 3

Author

Moreno-Manuel, Ana I, primary, Macías, Álvaro, additional, Cruz, Francisco M, additional, Gutiérrez, Lilian K, additional, Martínez, Fernando, additional, González-Guerra, Andrés, additional, Martínez Carrascoso, Isabel, additional, Bermúdez-Jimenez, Francisco José, additional, Sánchez-Pérez, Patricia, additional, Vera-Pedrosa, María Linarejos, additional, Ruiz, Juan Manuel, additional, Bernal, Juan A, additional, and Jalife, José, additional

Published
2024
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11. The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of short QT syndrome type 3.

Author

Moreno-Manuel, Ana I, Macías, Álvaro, Cruz, Francisco M, Gutiérrez, Lilian K, Martínez, Fernando, González-Guerra, Andrés, Carrascoso, Isabel Martínez, Bermúdez-Jimenez, Francisco José, Sánchez-Pérez, Patricia, Vera-Pedrosa, María Linarejos, Ruiz-Robles, Juan Manuel, Bernal, Juan A, and Jalife, José

Subjects
ATRIAL fibrillation, ARRHYTHMIA, VENTRICULAR arrhythmia, LABORATORY mice, ANIMAL disease models, ACTION potentials
Abstract

Aims Short QT syndrome type 3 (SQTS3) is a rare arrhythmogenic disease caused by gain-of-function mutations in KCNJ2 , the gene coding the inward rectifier potassium channel Kir2.1. We used a multidisciplinary approach and investigated arrhythmogenic mechanisms in an in-vivo model of de-novo mutation Kir2.1E299V identified in a patient presenting an extremely abbreviated QT interval and paroxysmal atrial fibrillation. Methods and results We used intravenous adeno-associated virus-mediated gene transfer to generate mouse models, and confirmed cardiac-specific expression of Kir2.1WT or Kir2.1E299V. On ECG, the Kir2.1E299V mouse recapitulated the QT interval shortening and the atrial-specific arrhythmia of the patient. The PR interval was also significantly shorter in Kir2.1E299V mice. Patch-clamping showed extremely abbreviated action potentials in both atrial and ventricular Kir2.1E299V cardiomyocytes due to a lack of inward-going rectification and increased IK1 at voltages positive to −80 mV. Relative to Kir2.1WT, atrial Kir2.1E299V cardiomyocytes had a significantly reduced slope conductance at voltages negative to −80 mV. After confirming a higher proportion of heterotetrameric Kir2.x channels containing Kir2.2 subunits in the atria, in-silico 3D simulations predicted an atrial-specific impairment of polyamine block and reduced pore diameter in the Kir2.1E299V-Kir2.2WT channel. In ventricular cardiomyocytes, the mutation increased excitability by shifting INa activation and inactivation in the hyperpolarizing direction, which protected the ventricle against arrhythmia. Moreover, Purkinje myocytes from Kir2.1E299V mice manifested substantially higher INa density than Kir2.1WT, explaining the abbreviation in the PR interval. Conclusion The first in-vivo mouse model of cardiac-specific SQTS3 recapitulates the electrophysiological phenotype of a patient with the Kir2.1E299V mutation. Kir2.1E299V eliminates rectification in both cardiac chambers but protects against ventricular arrhythmias by increasing excitability in both Purkinje-fiber network and ventricles. Consequently, the predominant arrhythmias are supraventricular likely due to the lack of inward rectification and atrial-specific reduced pore diameter of the Kir2.1E299V-Kir2.2WT heterotetramer. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Time-efficient three-dimensional transmural scar assessment provides relevant substrate characterization for ventricular tachycardia features and long-term recurrences in ischemic cardiomyopathy

Author

Merino-Caviedes, Susana, Gutierrez, Lilian K., Alfonso-Almazán, José Manuel, Sanz-Estébanez, Santiago, Cordero-Grande, Lucilio, Quintanilla, Jorge G., Sánchez-González, Javier, Marina-Breysse, Manuel, Galán-Arriola, Carlos, Enríquez-Vázquez, Daniel, Torres, Carlos, Pizarro, Gonzalo, Ibáñez, Borja, Peinado, Rafael, Merino, Jose Luis, Pérez-Villacastín, Julián, Jalife, José, López-Yunta, Mariña, Vázquez, Mariano, Aguado-Sierra, Jazmín, González-Ferrer, Juan José, Pérez-Castellano, Nicasio, Martín-Fernández, Marcos, Alberola-López, Carlos, and Filgueiras-Rama, David

Published
2021
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14. Tbx20 controls the expression of the KCNH2 gene and of hERG channels

Author

Caballero, Ricardo, Utrilla, Raquel G., Amorós, Irene, Matamoros, Marcos, Pérez-Hernández, Marta, Tinaquero, David, Alfayate, Silvia, Nieto-Marín, Paloma, Guerrero-Serna, Guadalupe, Liu, Qing-hua, Ramos-Mondragón, Roberto, Ponce-Balbuena, Daniela, Herron, Todd, Campbell, Katherine F., Filgueiras-Rama, David, Peinado, Rafael, López-Sendón, José L., Jalife, José, Delpón, Eva, and Tamargo, Juan

Published
2017

15. Extracellular cysteine disulfide bond break at Cys122 disrupts PIP2-dependent Kir2.1 channel function and leads to arrhythmias in Andersen-Tawil Syndrome

Author

Cruz, Francisco M., primary, Macías, Álvaro, additional, Moreno-Manuel, Ana I., additional, Gutiérrez, Lilian K., additional, Vera-Pedrosa, María Linarejos, additional, Martínez-Carrascoso, Isabel, additional, Pérez, Patricia Sánchez, additional, Ruiz Robles, Juan Manuel, additional, Bermúdez-Jiménez, Francisco J, additional, Díaz-Agustín, Aitor, additional, Martínez de Benito, Fernando, additional, Santiago, Salvador Arias, additional, Braza-Boils, Aitana, additional, Martín-Martínez, Mercedes, additional, Gutierrez-Rodríguez, Marta, additional, Bernal, Juan A., additional, Zorio, Esther, additional, Jiménez-Jaimez, Juan, additional, and Jalife, José, additional

Published
2023
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16. Cardiac electrical defects in progeroid mice and Hutchinson–Gilford progeria syndrome patients with nuclear lamina alterations

Author

Rivera-Torres, José, Calvo, Conrado J., Llach, Anna, Guzmán-Martínez, Gabriela, Caballero, Ricardo, González-Gómez, Cristina, Jiménez-Borreguero, Luis J., Guadix, Juan A., Osorio, Fernando G., López-Otín, Carlos, Herraiz-Martínez, Adela, Cabello, Nuria, Vallmitjana, Alex, Benítez, Raul, Gordon, Leslie B., Jalife, José, Pérez-Pomares, José M., Tamargo, Juan, Delpón, Eva, Hove-Madsen, Leif, Filgueiras-Rama, David, and Andrés, Vicente

Published
2016

23. Biobank-driven genomic discovery yields new insight into atrial fibrillation biology

Author

Nielsen, Jonas B., Thorolfsdottir, Rosa B., Fritsche, Lars G., Zhou, Wei, Skov, Morten W., Graham, Sarah E., Herron, Todd J., McCarthy, Shane, Schmidt, Ellen M., Sveinbjornsson, Gardar, Surakka, Ida, Mathis, Michael R., Yamazaki, Masatoshi, Crawford, Ryan D., Gabrielsen, Maiken E., Skogholt, Anne Heidi, Holmen, Oddgeir L., Lin, Maoxuan, Wolford, Brooke N., Dey, Rounak, Dalen, Håvard, Sulem, Patrick, Chung, Jonathan H., Backman, Joshua D., Arnar, David O., Thorsteinsdottir, Unnur, Baras, Aris, O’Dushlaine, Colm, Holst, Anders G., Wen, Xiaoquan, Hornsby, Whitney, Dewey, Frederick E., Boehnke, Michael, Kheterpal, Sachin, Mukherjee, Bhramar, Lee, Seunggeun, Kang, Hyun M., Holm, Hilma, Kitzman, Jacob, Shavit, Jordan A., Jalife, José, Brummett, Chad M., Teslovich, Tanya M., Carey, David J., Gudbjartsson, Daniel F., Stefansson, Kari, Abecasis, Gonçalo R., Hveem, Kristian, and Willer, Cristen J.

Published
2018
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24. Intermediate molecular phenotypes to identify genetic markers of anthracycline-induced cardiotoxicity risk

Author

Gómez-Vecino, Aurora, primary, Corchado-Cobos, Roberto, additional, Blanco-Gómez, Adrián, additional, García-Sancha, Natalia, additional, Castillo-Lluva, Sonia, additional, Martín-García, Ana, additional, Mendiburu-Eliçabe, Marina, additional, Prieto, Carlos, additional, Ruiz-Pinto, Sara, additional, Pita, Guillermo, additional, Velasco-Ruiz, Alejandro, additional, Patino-Alonso, Carmen, additional, Galindo-Villardón, Purificación, additional, Vera-Pedrosa, María Linarejos, additional, Jalife, José, additional, Mao, Jian-Hua, additional, de Plasencia, Guillermo Macías, additional, Castellanos-Martín, Andrés, additional, del Mar Sáez Freire, María, additional, Fraile-Martín, Susana, additional, Rodrigues-Teixeira, Telmo, additional, García-Macías, Carmen, additional, Galvis-Jiménez, Julie Milena, additional, García-Sánchez, Asunción, additional, Isidoro-García, María, additional, Fuentes, Manuel, additional, García-Cenador, María Begoña, additional, García-Criado, Francisco Javier, additional, García, Juan Luis, additional, Hernández-García, María Ángeles, additional, Cruz Hernández, Juan Jesús, additional, Rodríguez-Sánchez, César Augusto, additional, Martín-Ruiz, Alejandro, additional, Pérez-López, Estefanía, additional, Pérez-Martínez, Antonio, additional, Gutiérrez-Larraya, Federico, additional, Cartón, Antonio J., additional, García-Sáenz, José Ángel, additional, Patiño-García, Ana, additional, Martín, Miguel, additional, Gordoa, Teresa Alonso, additional, Vulsteke, Christof, additional, Croes, Lieselot, additional, Hatse, Sigrid, additional, Van Brussel, Thomas, additional, Lambrechts, Diether, additional, Wildiers, Hans, additional, Hang, Chang, additional, Holgado-Madruga, Marina, additional, González-Neira, Anna, additional, Sánchez, Pedro L, additional, and Pérez Losada, Jesús, additional

Published
2023
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26. Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes

Author

Takemoto, Yoshio, Ramirez, Rafael J., Yokokawa, Miki, Kaur, Kuljeet, Ponce-Balbuena, Daniela, Sinno, Mohamad C., Willis, B. Cicero, Ghanbari, Hamid, Ennis, Steven R., Guerrero-Serna, Guadalupe, Henzi, Bettina C., Latchamsetty, Rakesh, Ramos-Mondragon, Roberto, Musa, Hassan, Martins, Raphael P., Pandit, Sandeep V., Noujaim, Sami F., Crawford, Thomas, Jongnarangsin, Krit, Pelosi, Frank, Bogun, Frank, Chugh, Aman, Berenfeld, Omer, Morady, Fred, Oral, Hakan, and Jalife, José

Published
2016
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32. Lesion Index Titration Using Contact-Force Technology Enables Safe and Effective Radiofrequency Lesion Creation at the Root of the Aorta and Pulmonary Artery

Author

Alfonso-Almazán, José Manuel, Quintanilla, Jorge G., García-Torrent, María Jesús, Laguna-Castro, Santiago, Rodríguez-Bobada, Cruz, González, Pablo, González-Ferrer, Juan José, Salinas, Pablo, Cañadas-Godoy, Victoria, Moreno, Javier, Borrego-Bernabé, Luis, Pérez-Castellano, Nicasio, Jalife, José, Perez-Villacastín, Julián, and Filgueiras-Rama, David

Published
2019
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34. Contributors

Author

Aagaard, Philip, primary, Abrams, Dominic James, additional, Abriel, Hugues, additional, Adkisson, Wayne O., additional, Agullo-Pascual, Esperanza, additional, Alvarado, Francisco J., additional, Amin, Ahmad S., additional, Antzelevitch, Charles, additional, Anumonwo, Justus M.B., additional, Armaganijan, Luciana, additional, Arya, Arash, additional, Asirvatham, Samuel, additional, Atienza, Felipe, additional, Backx, Peter H., additional, Ballou, Lisa M., additional, Balse, Elise, additional, Balulad, Sujata, additional, Barbuti, Andrea, additional, Bardy, Gust H., additional, Bassil, Guillaume, additional, Benditt, David G., additional, Berenfeld, Omer, additional, Bers, Donald M., additional, Binah, Ofer, additional, Bogun, Frank, additional, Bongianino, Rossana, additional, Boyle, Noel G., additional, Boyle, Patrick M., additional, Breithardt, Günter, additional, Brini, Marisa, additional, Brink, Peter R., additional, Brugada, Pedro, additional, Buch, Eric, additional, Bukauskas, Feliksas F., additional, Calkins, Hugh, additional, Callans, David J., additional, Caples, Sean M., additional, Carafoli, Ernesto, additional, Catterall, William A., additional, Cerrone, Marina, additional, Chaumeil, Arnaud, additional, Chen, Caressa, additional, Chen, Lan S., additional, Chen, Peng-Sheng, additional, Cheng, Jianding, additional, Chiamvimonvat, Nipavan, additional, Christini, David J., additional, Chugh, Aman, additional, Climent, Andreu M., additional, Cohen, Ira S., additional, Connolly, Stuart J., additional, Cooper, Lebron, additional, Crespo, Eric M., additional, Crotti, Lia, additional, Csepe, Thomas A., additional, Cuoco, Frank, additional, Curtis, Anne B., additional, Damiano, Ralph J., additional, Darbar, Dawood, additional, Das, Mithilesh K., additional, d’Avila, Andre, additional, Delmar, Mario, additional, Delpón, Eva, additional, Denegri, Marco, additional, Denis, Arnaud, additional, Derval, Nicolas, additional, Deschênes, Isabelle, additional, Deshmukh, Abhishek, additional, Di Biase, Luigi, additional, Dickfeld, Timm M., additional, Dierckx, Hans, additional, Dinov, Borislav, additional, Dixit, Sanjay, additional, Dobrev, Dobromir, additional, Dubois, Remi, additional, Eckardt, Lars, additional, Edwards, Andrew G., additional, Ellenbogen, Kenneth A., additional, Ellinor, Patrick T., additional, Estes, N.A. Mark, additional, Fabritz, Larissa, additional, Fedorov, Vadim V., additional, Fernandez, Antonio B., additional, Teijeira Fernández, Elvis, additional, Filgueiras-Rama, David, additional, Fishbein, Michael C., additional, Fishman, Glenn I., additional, Frankel, David S., additional, Friedman, Paul, additional, Frontera, Antonio, additional, Gami, Apoor S., additional, Garabelli, Paul, additional, George, Alfred L., additional, Gerstenfeld, Edward P., additional, Gizurarson, Sigfus, additional, Gold, Michael R., additional, Goldberger, Jeffrey J., additional, Grace, Andrew, additional, Grassi, Guido, additional, Greenfield, Ruth Ann, additional, Gross, Wendy L., additional, Grubb, Blair P., additional, Guillem, María S., additional, Györke, Sándor, additional, Haïssaguerre, Michel, additional, Hake, Johan, additional, Halperin, Henry R., additional, Hansen, Brian J., additional, Hatem, Stéphane, additional, Hayes, David L., additional, Heijman, Jordi, additional, Herron, Todd J., additional, Hindricks, Gerhard, additional, Hocini, Mélèze, additional, Hohnloser, Stefan H., additional, Holmes, David R., additional, Hoshijima, Masahiko, additional, Hund, Thomas J., additional, Hutchinson, Mathew D., additional, Ilkhanoff, Leonard, additional, Ingles, Jodie, additional, Ip, James E., additional, Jackman, Warren M., additional, Jackson, Nicholas, additional, Jaïs, Pierre, additional, Jalife, José, additional, Jhun, Bong Sook, additional, John, Roy M., additional, Jongbloed, Monique, additional, Jordaens, Luc, additional, Kalman, Jonathan M., additional, Kamp, Timothy J., additional, Kanj, Mohamed H., additional, Kapa, Suraj, additional, Karabin, Beverly, additional, Karakikes, Ioannis, additional, Katritsis, Demosthenes G., additional, Kaur, Kuljeet, additional, Kirchhof, Paulus, additional, Kléber, André G., additional, Klein, George J., additional, Kohl, Peter, additional, Koneru, Jayanthi N., additional, Koruth, Jacob S., additional, Krahn, Andrew D., additional, Krogh-Madsen, Trine, additional, Kuck, Karl Heinz, additional, Kumar, Saurabh, additional, Kushnir, Alexander, additional, Lakdawala, Neal K., additional, Laksman, Zachary W.M., additional, Latchamsetty, Rakesh, additional, Lau, Dennis H., additional, Lerman, Bruce B., additional, Lin, Richard Z., additional, Lin, Shien-Fong, additional, Link, Mark S., additional, Liu, Bin, additional, Liu, Christopher F., additional, Lockwood, Deborah J., additional, Lopatin, Anatoli N., additional, Lubitz, Steven A., additional, Mahajan, Rajiv, additional, Makielski, Jonathan C., additional, Malik, Marek, additional, Marchlinski, Francis E., additional, Markowitz, Steven M., additional, Maron, Barry J., additional, Maron, Martin S., additional, Marx, Steven O., additional, Massé, Stéphane, additional, McCulloch, Andrew D., additional, McKelvie-Sebileau, Pippa, additional, Melby, Spencer J., additional, Metzner, Andreas, additional, Michailova, Anushka P., additional, Michaud, Gregory F., additional, Miller, John M., additional, Mishra, Jyotsna, additional, Mitrani, Raul D., additional, Mohler, Peter J., additional, Morady, Fred, additional, Myerburg, Robert J., additional, Nakagawa, Hiroshi, additional, Nalliah, Chrishan Joseph, additional, Nanthakumar, Kumaraswamy, additional, Napolitano, Carlo, additional, Narayan, Sanjiv M., additional, Natale, Andrea, additional, Nattel, Stanley, additional, Nazarian, Saman, additional, Nguyen, Thao P., additional, Nogami, Akihiko, additional, Noujaim, Sami F., additional, Nubret Le Coniat, Karine, additional, Olshansky, Brian, additional, O-Uchi, Jin, additional, Oudit, Gavin Y., additional, Ouyang, Feifan, additional, Ozcan, Cevher, additional, Packer, Douglas L., additional, Pandit, Sandeep V., additional, Panfilov, Alexander V., additional, Park, David S., additional, Patocskai, Bence, additional, Pauza, Dainius H., additional, Pauziene, Neringa, additional, Piccini, Jonathan P., additional, Pitt, Geoffrey S., additional, Po, Sunny S., additional, Prasad, Abhiram, additional, Priori, Silvia G., additional, Radwański, Przemysław B., additional, Rappel, Wouter-Jan, additional, Reiser, Michelle, additional, Restrepo, Alejandro Jimenez, additional, Robinson, Richard B., additional, Roden, Dan M., additional, Rosen, Michael R., additional, Rosso, Raphael, additional, Rudy, Yoram, additional, Rysevaite-Kyguoliene, Kristina, additional, Sabbah, Hani N., additional, Sacher, Frederic, additional, Sachse, Frank B., additional, Saguner, Ardan M., additional, Sanders, Prashanthan, additional, Sanguinetti, Michael C., additional, Santangeli, Pasquale, additional, Sarraf, Mohammad, additional, Satin, Jonathan, additional, Schalij, Martin Jan, additional, Scherlag, Benjamin J., additional, Schill, Matthew R., additional, Schleifer, J. William, additional, Schuessler, Richard B., additional, Schwartz, Peter J., additional, Seeger, Timon, additional, Semsarian, Christopher, additional, Seravalle, Gino, additional, Shah, Ashok J., additional, Shaw, Robin M., additional, Shen, Mark J., additional, Shen, Win–Kuang, additional, Sheu, Shey-Shing, additional, Shivkumar, Kalyanam, additional, Silva, Jennifer N.A., additional, Skanes, Allan C., additional, Soejima, Kyoko, additional, Somers, Virend K., additional, Sorajja, Dan, additional, Stavrakis, Stavros, additional, Steinberg, Christian, additional, Stevenson, Lynne Warner, additional, Stevenson, William G., additional, Sweeney, Michael O., additional, Swerdlow, Charles, additional, Takigawa, Masateru, additional, Tamargo, Juan, additional, Tandri, Harikrishna, additional, Tedrow, Usha B., additional, Thompson, Nathaniel, additional, Thompson, Paul D., additional, Tomaselli, Gordon F., additional, Towbin, Jeffrey A., additional, Trayanova, Natalia A., additional, Tristani-Firouzi, Martin, additional, Tseng, Zian H., additional, Ueda, Akiko, additional, Valdivia, Héctor H., additional, Valiunas, Virginijus, additional, van der Werf, Christian, additional, Van Hare, George F., additional, Vidmar, David, additional, Viskin, Sami, additional, Voigt, Niels, additional, Walsh, Edward P., additional, Wang, Paul J., additional, Wehrens, Xander H.T., additional, Weiss, Mark S., additional, Wilde, Arthur A.M., additional, Wilkoff, Bruce L., additional, Woo, Y. Joseph, additional, Wu, Joseph C., additional, Yee, Raymond, additional, Zaman, Junaid A.B., additional, Zarzoso, Manuel, additional, Zeitler, Emily P., additional, Zeppenfeld, Katja, additional, Zghaib, Tarek, additional, Zhang, Xiao-Dong, additional, and Zipes, Douglas P., additional

Published
2018
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36. Preface

Author

Zipes, Douglas P., primary, Jalife, José, additional, and Stevenson, William G., additional

Published
2018
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39. Spectral analysis-based risk score enables early prediction of mortality and cerebral performance in patients undergoing therapeutic hypothermia for ventricular fibrillation and comatose status

Author

Filgueiras-Rama, David, Calvo, Conrado J., Salvador-Montañés, Óscar, Cádenas, Rosalía, Ruiz-Cantador, Jose, Armada, Eduardo, Rey, Juan Ramón, Merino, J.L., Peinado, Rafael, Pérez-Castellano, Nicasio, Pérez-Villacastín, Julián, Quintanilla, Jorge G., Jiménez, Santiago, Castells, Francisco, Chorro, Francisco J., López-Sendón, J.L., Berenfeld, Omer, Jalife, José, de Sá, Esteban López, and Millet, José

Published
2015
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43. MKK6 deficiency promotes cardiac dysfunction through MKK3-p38γ/δ-mTOR hyperactivation

Author

Romero-Becerra, Rafael, primary, Mora, Alfonso, additional, Manieri, Elisa, additional, Nikolic, Ivana, additional, Santamans, Ayelén Melina, additional, Montalvo-Romeral, Valle, additional, Cruz, Francisco Miguel, additional, Rodríguez, Elena, additional, León, Marta, additional, Leiva-Vega, Luis, additional, Sanz, Laura, additional, Bondía, Víctor, additional, Filgueiras-Rama, David, additional, Jiménez-Borreguero, Luis Jesús, additional, Jalife, José, additional, Gonzalez-Teran, Barbara, additional, and Sabio, Guadalupe, additional

Published
2022
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45. Distinct spectral dynamics of implanted cardiac defibrillator signals in spontaneous termination of polymorphic ventricular tachycardia and fibrillation in patients with electrical and structural diseases

Author

Calvo, David, primary, Salinas, Lucia, additional, Martínez-Camblor, Pablo, additional, García-Iglesias, Daniel, additional, Alzueta, Javier, additional, Rodríguez, Anibal, additional, Romero, Rafael, additional, Viñolas, Xavier, additional, Fernández-Lozano, Ignacio, additional, Anguera, Ignasi, additional, Villacastín, Julián, additional, Bodegas, Andrés, additional, Fontenla, Adolfo, additional, Jalife, José, additional, and Berenfeld, Omer, additional

Published
2022
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47. Cardiac Kir2.1 and NaV1.5 Channels Traffic Together to the Sarcolemma to Control Excitability

Author

Ponce-Balbuena, Daniela, Guerrero-Serna, Guadalupe, Valdivia, Carmen R., Caballero, Ricardo, Diez-Guerra, F. Javier, Jiménez-Vázquez, Eric N., Ramírez, Rafael J., Monteiro da Rocha, André, Herron, Todd J., Campbell, Katherine F., Willis, B. Cicero, Alvarado, Francisco J., Zarzoso, Manuel, Kaur, Kuljeet, Pérez-Hernández, Marta, Matamoros, Marcos, Valdivia, Héctor H., Delpón, Eva, and Jalife, José

Published
2018
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50. Molecular stratification of arrhythmogenic mechanisms in the Andersen Tawil syndrome.

Author

Moreno-Manuel, Ana Isabel, Gutiérrez, Lilian K, Vera-Pedrosa, María Linarejos, Cruz, Francisco Miguel, Bermúdez-Jiménez, Francisco José, Martínez-Carrascoso, Isabel, Sánchez-Pérez, Patricia, Macías, Álvaro, and Jalife, José

Subjects
ARRHYTHMIA, CARDIAC arrest, VENTRICULAR tachycardia, SYMPTOMS, GENE expression, POTASSIUM channels
Abstract

Andersen-Tawil syndrome (ATS) is a rare inheritable disease associated with loss-of-function mutations in KCNJ2, the gene coding the strong inward rectifier potassium channel Kir2.1, which forms an essential membrane protein controlling cardiac excitability. ATS is usually marked by a triad of periodic paralysis, life-threatening cardiac arrhythmias and dysmorphic features, but its expression is variable and not all patients with a phenotype linked to ATS have a known genetic alteration. The mechanisms underlying this arrhythmogenic syndrome are poorly understood. Knowing such mechanisms would be essential to distinguish ATS from other channelopathies with overlapping phenotypes and to develop individualized therapies. For example, the recently suggested role of Kir2.1 as a countercurrent to sarcoplasmic calcium reuptake might explain the arrhythmogenic mechanisms of ATS and its overlap with catecholaminergic polymorphic ventricular tachycardia. Here we summarize current knowledge on the mechanisms of arrhythmias leading to sudden cardiac death in ATS. We first provide an overview of the syndrome and its pathophysiology, from the patient's bedside to the protein and discuss the role of essential regulators and interactors that could play a role in cases of ATS. The review highlights novel ideas related to some post-translational channel interactions with partner proteins that might help define the molecular bases of the arrhythmia phenotype. We then propose a new all-embracing classification of the currently known ATS loss-of-function mutations according to their position in the Kir2.1 channel structure and their functional implications. We also discuss specific ATS pathogenic variants, their clinical manifestations, and treatment stratification. The goal is to provide a deeper mechanistic understanding of the syndrome toward the development of novel targets and personalized treatment strategies. [ABSTRACT FROM AUTHOR]

Published
2023
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