Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Abstract

Cardiovascular diseases (CVDs) are currently the leading cause of death worldwide. In 2022, the CVDs contributed to 19.8 million deaths globally, accounting for one-third of all global deaths. With an aging population and changing lifestyles, CVDs pose a major threat to human health. Mitochondria-associated endoplasmic reticulum membranes (MAMs) are communication platforms between cellular organelles and regulate cellular physiological functions, including apoptosis, autophagy, and programmed necrosis. Further research has shown that MAMs play a critical role in the pathogenesis of CVDs, including myocardial ischemia and reperfusion injury, heart failure, pulmonary hypertension, and coronary atherosclerosis. This suggests that MAMs could be an important therapeutic target for managing CVDs. The goal of this study is to summarize the protein complex of MAMs, discuss its role in the pathological mechanisms of CVDs in terms of its functions such as Ca2+ transport, apoptotic signaling, and lipid metabolism, and suggest the possibility of MAMs as a potential therapeutic approach.

Mitofusin 2 inhibits high glucose-induced apoptosis of human lens epithelial cells via modulating mitochondrial function and autophagy

“…On the basis of these observations, we support that MFN2 plays a key role in restoring mitochondrial function in HG-induced HLE-B3 cells. In addition, mitochondria and endoplasmic reticulum (ER) are distinct organelles that physically interact with each other, including exchange of phospholipids, calcium and other metabolites to maintain cellular integrity and bioenergetics [31][32][33]. Previous studies have reported that MFN2 promotes the contact of mitochondria and ER [32,34,35].…”