Mitochondrial Ca
| Autor: | Hai-Xia, Xu, Su-Mei, Cui, Ying-Mei, Zhang, Jun, Ren |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Heart Failure
Mitophagy Apoptosis Intracellular Membranes Review Article Endoplasmic Reticulum Mitochondria Necrosis mitochondrial Ca2+ transport myocardial apoptosis Adenosine Triphosphate ATP synthesis ROS production mitochondrial Ca2+ homeostasis MAMs Animals Homeostasis Humans Calcium Reactive Oxygen Species |
| Zdroj: | Acta Pharmacologica Sinica |
| ISSN: | 1745-7254 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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