MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
| Autor: | Jing Zhou, Zhen Fan, Ai Guo, Yong-Xin Wu, Qian Xiao, Qiu-Nan Chen, Jiang-Hao Wu, Yun-Fei Yang, Zhiyin Liao, Wu Yang, Jing Yu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Mitochondrial ROS
Cancer Research Aging Sarcopenia Immunology chemistry.chemical_element Calcium medicine.disease_cause Mitochondrial Membrane Transport Proteins Article Antioxidants Cellular and Molecular Neuroscience Mice medicine Animals Humans Mitochondrial calcium uptake Muscle Skeletal QH573-671 Myogenesis Calcium-Binding Proteins Skeletal muscle Cell Biology medicine.disease Cell biology Ageing medicine.anatomical_structure chemistry Calcium and phosphate metabolic disorders Cytology Homeostasis Oxidative stress |
| Zdroj: | Cell Death & Disease Cell Death and Disease, Vol 12, Iss 12, Pp 1-13 (2021) |
| ISSN: | 2041-4889 |
| Popis: | Age-related loss of skeletal muscle mass and function, termed sarcopenia, could impair the quality of life in the elderly. The mechanisms involved in skeletal muscle aging are intricate and largely unknown. However, more and more evidence demonstrated that mitochondrial dysfunction and apoptosis also play an important role in skeletal muscle aging. Recent studies have shown that mitochondrial calcium uniporter (MCU)-mediated mitochondrial calcium affects skeletal muscle mass and function by affecting mitochondrial function. During aging, we observed downregulated expression of mitochondrial calcium uptake family member3 (MICU3) in skeletal muscle, a regulator of MCU, which resulted in a significant reduction in mitochondrial calcium uptake. However, the role of MICU3 in skeletal muscle aging remains poorly understood. Therefore, we investigated the effect of MICU3 on the skeletal muscle of aged mice and senescent C2C12 cells induced by d-gal. Downregulation of MICU3 was associated with decreased myogenesis but increased oxidative stress and apoptosis. Reconstitution of MICU3 enhanced antioxidants, prevented the accumulation of mitochondrial ROS, decreased apoptosis, and increased myogenesis. These findings indicate that MICU3 might promote mitochondrial Ca2+ homeostasis and function, attenuate oxidative stress and apoptosis, and restore skeletal muscle mass and function. Therefore, MICU3 may be a potential therapeutic target in skeletal muscle aging. |
| Databáze: | OpenAIRE |
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