MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging

Abstract 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 apop...

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Autores principales:	Yun-Fei Yang, Wu Yang, Zhi-Yin Liao, Yong-Xin Wu, Zhen Fan, Ai Guo, Jing Yu, Qiu-Nan Chen, Jiang-Hao Wu, Jing Zhou, Qian Xiao
Formato:	article
Lenguaje:	EN
Publicado:	Nature Publishing Group 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/7c6ff91c405845a5a2b25eb2ff947046
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spelling	oai:doaj.org-article:7c6ff91c405845a5a2b25eb2ff9470462021-12-05T12:04:21ZMICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging10.1038/s41419-021-04400-52041-4889https://doaj.org/article/7c6ff91c405845a5a2b25eb2ff9470462021-11-01T00:00:00Zhttps://doi.org/10.1038/s41419-021-04400-5https://doaj.org/toc/2041-4889Abstract 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.Yun-Fei YangWu YangZhi-Yin LiaoYong-Xin WuZhen FanAi GuoJing YuQiu-Nan ChenJiang-Hao WuJing ZhouQian XiaoNature Publishing GrouparticleCytologyQH573-671ENCell Death and Disease, Vol 12, Iss 12, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Yun-Fei Yang Wu Yang Zhi-Yin Liao Yong-Xin Wu Zhen Fan Ai Guo Jing Yu Qiu-Nan Chen Jiang-Hao Wu Jing Zhou Qian Xiao MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
description	Abstract 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.
format	article
author	Yun-Fei Yang Wu Yang Zhi-Yin Liao Yong-Xin Wu Zhen Fan Ai Guo Jing Yu Qiu-Nan Chen Jiang-Hao Wu Jing Zhou Qian Xiao
author_facet	Yun-Fei Yang Wu Yang Zhi-Yin Liao Yong-Xin Wu Zhen Fan Ai Guo Jing Yu Qiu-Nan Chen Jiang-Hao Wu Jing Zhou Qian Xiao
author_sort	Yun-Fei Yang
title	MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
title_short	MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
title_full	MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
title_fullStr	MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
title_full_unstemmed	MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging
title_sort	micu3 regulates mitochondrial ca2+-dependent antioxidant response in skeletal muscle aging
publisher	Nature Publishing Group
publishDate	2021
url	https://doaj.org/article/7c6ff91c405845a5a2b25eb2ff947046
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_version_	1718372264319123456

MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging

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