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Usage Information

Mitochondrial dysfunction in pathophysiology of heart failure
Bo Zhou, Rong Tian
Bo Zhou, Rong Tian
Published August 20, 2018
Citation Information: J Clin Invest. 2018;128(9):3716-3726. https://doi.org/10.1172/JCI120849.
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Review Series

Mitochondrial dysfunction in pathophysiology of heart failure

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Abstract

Mitochondrial dysfunction has been implicated in the development of heart failure. Oxidative metabolism in mitochondria is the main energy source of the heart, and the inability to generate and transfer energy has long been considered the primary mechanism linking mitochondrial dysfunction and contractile failure. However, the role of mitochondria in heart failure is now increasingly recognized to be beyond that of a failed power plant. In this Review, we summarize recent evidence demonstrating vicious cycles of pathophysiological mechanisms during the pathological remodeling of the heart that drive mitochondrial contributions from being compensatory to being a suicide mission. These mechanisms include bottlenecks of metabolic flux, redox imbalance, protein modification, ROS-induced ROS generation, impaired mitochondrial Ca2+ homeostasis, and inflammation. The interpretation of these findings will lead us to novel avenues for disease mechanisms and therapy.

Authors

Bo Zhou, Rong Tian

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Usage data is cumulative from February 2022 through February 2023.

Usage JCI PMC
Text version 11,229 1,734
PDF 1,669 603
Figure 1,372 81
Citation downloads 211 0
Totals 14,481 2,418
Total Views 16,899
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