Biology

Disuse-associated loss of the protease LONP1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass and strength

Z. Xu, T. Fu, et al.

This research reveals the crucial role of LONP1, a key mitochondrial protease, in maintaining mitochondrial function and preserving skeletal muscle mass and strength during muscle disuse. Conducted by Zhisheng Xu and colleagues, the study highlights how reduced levels of LONP1 are linked to muscle atrophy and strength loss, a finding that could pave the way for new therapies in muscle degeneration.

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Abstract

This study investigates the role of LONP1, a major mitochondrial protease, in regulating mitochondrial function and skeletal muscle mass and strength in response to muscle disuse. Researchers found that disuse-related muscle loss in mice and humans is associated with decreased mitochondrial LONP1 protein. Skeletal muscle-specific ablation of LONP1 in mice impaired mitochondrial protein turnover, leading to mitochondrial dysfunction, reduced muscle fiber size, and reduced strength. Overexpressing a mitochondrial-retained mutant protein also induced mitochondrial dysfunction and muscle loss. These findings highlight the importance of LONP1 in maintaining mitochondrial function and preserving skeletal muscle mass and strength.

Publisher

NATURE COMMUNICATIONS

Published On

Feb 16, 2022

Authors

Zhisheng Xu, Tingting Fu, Qiqi Guo, Danxia Zhou, Wanping Sun, Zheng Zhou, Xinyi Chen, Jingzi Zhang, Lin Liu, Liwei Xiao, Yujing Yin, Yuhuan Jia, Erkai Pang, Yuncong Chen, Xin Pan, Lei Fang, Min-sheng Zhu, Wenyong Fei, Bin Lu, Zhenji Gan

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