Endurance swimming exacerbates mitochondrial myopathy in mice with high mtDNA deletions.

IF 3.9 3区 生物学 Q2 CELL BIOLOGY Mitochondrion Pub Date : 2025-02-14 DOI:10.1016/j.mito.2025.102010
Sho Hanada, Kaori Ishikawa, Takanaga Shirai, Tohru Takemasa, Kazuto Nakada
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Abstract

Recent studies have reported that endurance exercise enhances mitochondrial function, facilitating discussions of its potential as a therapeutic strategy for mitochondrial diseases caused by the accumulation of mutant mitochondrial DNA (mtDNA). In this study, we assessed the effects of endurance exercise on muscle pathology in a mitochondrial disease mouse model (mito-miceΔ) that is characterized by severe clinical phenotypes owing to the predominant accumulation of mtDNA with a large-scale deletion (ΔmtDNA). Contrary to expectations that endurance exercise may enhance mitochondrial function, endurance exercise exacerbated muscle pathology in mito-miceΔ. Therefore, exercise interventions should be potentially avoided in patients with severe mitochondrial diseases.

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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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