Mitochondrial Ca2+ regulation in the etiology of heart failure: physiological and pathophysiological implications.

Acta Pharmacologica Sinica
Hai-Xia XuJun Ren

Abstract

Heart failure (HF) represents one of the leading causes of cardiovascular diseases with high rates of hospitalization, morbidity and mortality worldwide. Ample evidence has consolidated a crucial role for mitochondrial injury in the progression of HF. It is well established that mitochondrial Ca2+ participates in the regulation of a wide variety of biological processes, including oxidative phosphorylation, ATP synthesis, reactive oxygen species (ROS) generation, mitochondrial dynamics and mitophagy. Nonetheless, mitochondrial Ca2+ overload stimulates mitochondrial permeability transition pore (mPTP) opening and mitochondrial swelling, resulting in mitochondrial injury, apoptosis, cardiac remodeling, and ultimately development of HF. Moreover, mitochondria possess a series of Ca2+ transport influx and efflux channels, to buffer Ca2+ in the cytoplasm. Interaction at mitochondria-associated endoplasmic reticulum membranes (MAMs) may also participate in the regulation of mitochondrial Ca2+ homeostasis and plays an essential role in the progression of HF. Here, we provide an overview of regulation of mitochondrial Ca2+ homeostasis in maintenance of cardiac function, in an effort to identify novel therapeutic strategies for the manag...Continue Reading

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Citations

Dec 1, 2020·Frontiers in Physiology·Xue KongWei Ge
Feb 24, 2021·Nature Reviews. Cardiology·Jun RenYingmei Zhang
Mar 12, 2021·Endocrine Reviews·Amir AjoolabadyJun Ren
Jun 23, 2021·Biological Reviews of the Cambridge Philosophical Society·Giampaolo MorcianoPaulo J Oliveira
Jul 25, 2021·International Journal of Molecular Sciences·Xuan WangJunjie Luo
Aug 21, 2021·Journal of Analytical Methods in Chemistry·Vu Thi ThuNguyen Thi Ha Ly
May 6, 2021·Physiological Reviews·Jun RenYingmei Zhang

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Methods Mentioned

BETA
GTPase
acetylation

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