期刊
ACTA PHARMACOLOGICA SINICA
卷 41, 期 10, 页码 1301-1309出版社
NATURE PUBL GROUP
DOI: 10.1038/s41401-020-0476-5
关键词
heart failure; mitochondrial Ca(2+)homeostasis; mitochondrial Ca(2+)transport; MAMs; ATP synthesis; ROS production; myocardial apoptosis
资金
- National Natural Science Foundation of China [81770261, 91749128]
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 Ca(2+)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 Ca(2+)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 Ca(2+)transport influx and efflux channels, to buffer Ca(2+)in the cytoplasm. Interaction at mitochondria-associated endoplasmic reticulum membranes (MAMs) may also participate in the regulation of mitochondrial Ca(2+)homeostasis and plays an essential role in the progression of HF. Here, we provide an overview of regulation of mitochondrial Ca(2+)homeostasis in maintenance of cardiac function, in an effort to identify novel therapeutic strategies for the management of HF.
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