期刊
出版社
MDPI
DOI: 10.3390/ijerph18083874
关键词
mitochondria-associated membrane; endo; sarcoplasmic reticulum-mitochondria Ca2+ transport; mitochondrial calcium overload; skeletal muscle function
资金
- National Natural Science Foundation of China [31471133]
- Fundamental Research Funds for the Central Universities [2019PT013, 2020025]
The mitochondria-associated membrane (MAM) serves as a crucial platform for regulating various cellular processes and diseases. Evidence suggests that alterations in Ca2+ transport may be a universal mechanism for ER-mitochondria cross-talk in different physiological/pathological conditions.
The physical contact site between a mitochondrion and endoplasmic reticulum (ER), named the mitochondria-associated membrane (MAM), has emerged as a fundamental platform for regulating the functions of the two organelles and several cellular processes. This includes Ca2+ transport from the ER to mitochondria, mitochondrial dynamics, autophagy, apoptosis signalling, ER stress signalling, redox reaction, and membrane structure maintenance. Consequently, the MAM is suggested to be involved in, and as a possible therapeutic target for, some common diseases and impairment in skeletal muscle function, such as insulin resistance and diabetes, obesity, neurodegenerative diseases, Duchenne muscular dystrophy, age-related muscle atrophy, and exercise-induced muscle damage. In the past decade, evidence suggests that alterations in Ca2+ transport from the ER to mitochondria, mediated by the macromolecular complex formed by IP3R, Grp75, and VDAC1, may be a universal mechanism for how ER-mitochondria cross-talk is involved in different physiological/pathological conditions mentioned above. A better understanding of the ER (or sarcoplasmic reticulum in muscle)-mitochondria Ca2+ transport system may provide a new perspective for exploring the mechanism of how the MAM is involved in the pathology of diseases and skeletal muscle dysfunction. This review provides a summary of recent research findings in this area.
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