Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 61, Issue 6, Pages 599-610Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2012.08.1021
Keywords
cardiomyocytes; heart failure; mitochondria
Categories
Funding
- National Institutes of Health [K02 HL107448, R01 HL104181, 1P01 HL108795]
- Bayer Schering Pharma AG
- Debio-Pharm S.A.
- Medtronic
- Novartis Pharma AG
- Otsuka Pharmaceuticals
- Sigma Tau
- Solvay Pharmaceuticals
- Sticares InterACT
- Takeda Pharmaceuticals North America, Inc.
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Heart failure is a pressing public health problem with no curative treatment currently available. The existing therapies provide symptomatic relief, but are unable to reverse molecular changes that occur in cardiomyocytes. The mechanisms of heart failure are complex and multiple, but mitochondrial dysfunction appears to be a critical factor in the development of this disease. Thus, it is important to focus research efforts on targeting mitochondrial dysfunction in the failing heart to revive the myocardium and its contractile function. This review highlights the 3 promising areas for the development of heart failure therapies, including mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial iron handling. Moreover, the translational potential of compounds targeting these pathways is discussed. (J Am Coll Cardiol 2013;61:599-610) (C) 2013 by the American College of Cardiology Foundation
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