Mitochondrial Dysfunction in Myoblasts: A TSPO-Dependent Mechanism of Sarcopenia

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ID: 315592
2026
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Abstract
Sarcopenia, the age-related loss of muscle mass and function, poses a significant health burden in aging societies. Although mitochondrial dysfunction is a recognized driver, the upstream molecular regulators remain poorly defined. Here, we identify the mitochondrial translocator protein (TSPO) as a novel negative regulator of myogenesis that is consistently upregulated in aged and sarcopenic muscle. Using gain- and loss-of-function approaches in C2C12 myoblasts, we show that TSPO overexpression disrupts mitochondrial homeostasis, impairs proliferation and differentiation, while TSPO knockdown produces opposite effects-establishing TSPO as a critical modulator of myogenic capacity. Mechanistically, TSPO suppresses the Wnt/β-catenin pathway, and this effect is partially mediated by ROS accumulation. Importantly, in vivo AAV9-mediated TSPO knockdown in aged mice not only restores mitochondrial integrity but also significantly improves muscle mass, strength, and exercise performance. Collectively, our findings uncover a TSPO-Wnt/β-catenin axis that links mitochondrial dysfunction to impaired muscle regeneration in aging. Targeting TSPO may offer a dual-action therapeutic strategy to combat sarcopenia by simultaneously enhancing mitochondrial bioenergetics and reactivating pro-myogenic signaling.
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Authors Peng Zhang, Hongyu Zheng, Zhao Lin, Hanhao Dai, Minjuan Zhang, L Y Yang, Zhibo Deng, Chao Song, Yibin Su, R Zhang, Guoyu Yu, Jun Luo, J Q Xu, Fenqi Luo
Journal the journals of gerontology series a, biological sciences and medical sciences
Year 2026
DOI
10.1093/gerona/glag145
URL
https://doi.org/10.1093/gerona/glag145
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