Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis

Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis

The authors found that VDAC2 plays a crucial role in influencing mitochondrial calcium dynamics and cellular calcium signalling. A VDAC2 agonist, efsevin, rescued the heart failure phenotype, identifying a new potential therapeutic target for heart failure.

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Detalles Bibliográficos
Autores principales: Thirupura S. Shankar, Dinesh K. A. Ramadurai, Kira Steinhorst, Salah Sommakia, Rachit Badolia, Aspasia Thodou Krokidi, Dallen Calder, Sutip Navankasattusas, Paulina Sander, Oh Sung Kwon, Aishwarya Aravamudhan, Jing Ling, Andreas Dendorfer, Changmin Xie, Ohyun Kwon, Emily H. Y. Cheng, Kevin J. Whitehead, Thomas Gudermann, Russel S. Richardson, Frank B. Sachse, Johann Schredelseker, Kenneth W. Spitzer, Dipayan Chaudhuri, Stavros G. Drakos
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
Science
Q
Acceso en línea:https://doaj.org/article/5def0b8a41bf407088eed68a7df3942d
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Descripción
Sumario:The authors found that VDAC2 plays a crucial role in influencing mitochondrial calcium dynamics and cellular calcium signalling. A VDAC2 agonist, efsevin, rescued the heart failure phenotype, identifying a new potential therapeutic target for heart failure.

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