Details

Autor(en) / Beteiligte

• Xu, Hai-Xia
• Cui, Su-Mei
• Zhang, Ying-Mei
• Ren, Jun

Titel

Mitochondrial Ca 2+ regulation in the etiology of heart failure: physiological and pathophysiological implications

Ist Teil von

• Acta pharmacologica Sinica, 2020-10, Vol.41 (10), p.1301

Ort / Verlag

United States

Erscheinungsjahr

2020

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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 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 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 transport influx and efflux channels, to buffer Ca in the cytoplasm. Interaction at mitochondria-associated endoplasmic reticulum membranes (MAMs) may also participate in the regulation of mitochondrial Ca homeostasis and plays an essential role in the progression of HF. Here, we provide an overview of regulation of mitochondrial Ca homeostasis in maintenance of cardiac function, in an effort to identify novel therapeutic strategies for the management of HF.