Nature Communications (Jul 2021)
Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis
- 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
Affiliations
- Thirupura S. Shankar
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Dinesh K. A. Ramadurai
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Kira Steinhorst
- Walther Straub Institute of Pharmacology and Toxicology, Faculty of Medicine, LMU Munich
- Salah Sommakia
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Rachit Badolia
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Aspasia Thodou Krokidi
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Dallen Calder
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Sutip Navankasattusas
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Paulina Sander
- Walther Straub Institute of Pharmacology and Toxicology, Faculty of Medicine, LMU Munich
- Oh Sung Kwon
- Department of Kinesiology, University of Connecticut
- Aishwarya Aravamudhan
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Jing Ling
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Andreas Dendorfer
- Walter-Brendel-Center of Experimental Medicine, Ludwig-Maximilians Universität Munich
- Changmin Xie
- Department of Chemistry and Biochemistry, University of California
- Ohyun Kwon
- Department of Chemistry and Biochemistry, University of California
- Emily H. Y. Cheng
- Memorial Sloan Kettering Cancer Center
- Kevin J. Whitehead
- Division of Cardiovascular Medicine, University of Utah School of Medicine
- Thomas Gudermann
- Walther Straub Institute of Pharmacology and Toxicology, Faculty of Medicine, LMU Munich
- Russel S. Richardson
- Geriatric Research, Education, and Clinical Center, Salt Lake City VA Medical Center
- Frank B. Sachse
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Johann Schredelseker
- Walther Straub Institute of Pharmacology and Toxicology, Faculty of Medicine, LMU Munich
- Kenneth W. Spitzer
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Dipayan Chaudhuri
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- Stavros G. Drakos
- Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah
- DOI
- https://doi.org/10.1038/s41467-021-24869-0
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 15
Abstract
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.
