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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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10.1038/s41401-020-0476-5
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document_parses/pdf_json/0d20fe2cb44fc7949ea2d8f2d97dc0dc2f35f8c1.json
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document_parses/pmc_json/PMC7608470.xml.json
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Mitochondrial Ca(2+) regulation in the etiology of heart failure: physiological and pathophysiological implications
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