Mitochondrial dysfunction in pathophysiology of heart failure

By Bo Zhou, Rong Tian. Journal of Clinical Investigation, 2018

753 citations recorded by the source corpus.

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.

Subfields: Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d5457eb9e9dfb379bbc005268f99f8801304fe20

How researchers see this paper

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In Clinical Biochemistry

1. Yan Pang
2. Xianqun Fan
3. Xieyang Xu

In Molecular Biology

1. S. Verma
2. Yan Pang
3. Xianqun Fan
4. Xieyang Xu

Citations in the corpus

• Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors (2020, background): “In diabetic mice, increasing glycemic control with SGLT2 inhibition can decrease myocardial ROS production and cardiac fibrosis (97).”
• Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “27,28,333 In the process of mitochondrial dysfunction, imbalanced ROS production and subsequent oxidative stress play an important role, leading to cardiac injury.”