Nature Communications (Sep 2020)
Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
- Elizabeth D. Luczak,
- Yuejin Wu,
- Jonathan M. Granger,
- Mei-ling A. Joiner,
- Nicholas R. Wilson,
- Ashish Gupta,
- Priya Umapathi,
- Kevin R. Murphy,
- Oscar E. Reyes Gaido,
- Amin Sabet,
- Eleonora Corradini,
- Wen-Wei Tseng,
- Yibin Wang,
- Albert J. R. Heck,
- An-Chi Wei,
- Robert G. Weiss,
- Mark E. Anderson
Affiliations
- Elizabeth D. Luczak
- Department of Medicine, The Johns Hopkins University School of Medicine
- Yuejin Wu
- Department of Medicine, The Johns Hopkins University School of Medicine
- Jonathan M. Granger
- Department of Medicine, The Johns Hopkins University School of Medicine
- Mei-ling A. Joiner
- Department of Internal Medicine, University of Iowa Carver College of Medicine
- Nicholas R. Wilson
- Department of Medicine, The Johns Hopkins University School of Medicine
- Ashish Gupta
- Department of Medicine, The Johns Hopkins University School of Medicine
- Priya Umapathi
- Department of Medicine, The Johns Hopkins University School of Medicine
- Kevin R. Murphy
- Department of Medicine, The Johns Hopkins University School of Medicine
- Oscar E. Reyes Gaido
- Department of Medicine, The Johns Hopkins University School of Medicine
- Amin Sabet
- Department of Medicine, The Johns Hopkins University School of Medicine
- Eleonora Corradini
- Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University
- Wen-Wei Tseng
- Department of Electrical Engineering, Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University
- Yibin Wang
- Departments of Anesthesiology, Physiology and Medicine, David Geffen School of Medicine, University of California
- Albert J. R. Heck
- Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University
- An-Chi Wei
- Department of Medicine, The Johns Hopkins University School of Medicine
- Robert G. Weiss
- Department of Medicine, The Johns Hopkins University School of Medicine
- Mark E. Anderson
- Department of Medicine, The Johns Hopkins University School of Medicine
- DOI
- https://doi.org/10.1038/s41467-020-18165-6
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 18
Abstract
Little is known about how cardiac metabolism remodels following cardiac injury. Here, the authors show that mitochondrial CaMKII plays an important role in remodeling cardiac metabolism after injury and that replacement of mitochondrial creatine kinase improves energetics and protects against adverse remodeling.
