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

   
@article{APS10208,
	author = {Hai-xia Xu and Su-mei Cui and Ying-mei Zhang and Jun Ren},
	title = {Mitochondrial Ca2+ regulation in the etiology of heart failure: physiological and pathophysiological implications},
	journal = {Acta Pharmacologica Sinica},
	volume = {41},
	number = {10},
	year = {2020},
	keywords = {},
	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 management of HF.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/10208}
}