耐力游泳加剧线粒体肌病小鼠高mtDNA缺失。

IF 4.5 3区 生物学 Q2 CELL BIOLOGY
Sho Hanada , Kaori Ishikawa , Takanaga Shirai , Tohru Takemasa , Kazuto Nakada
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引用次数: 0

摘要

最近的研究报道,耐力运动增强了线粒体功能,促进了其作为由突变线粒体DNA (mtDNA)积累引起的线粒体疾病的治疗策略的潜力的讨论。在这项研究中,我们在线粒体疾病小鼠模型(mito-miceΔ)中评估了耐力运动对肌肉病理的影响,该模型的特点是由于mtDNA的主要积累和大规模缺失(ΔmtDNA)导致严重的临床表型。与耐力运动可能增强线粒体功能的预期相反,耐力运动加剧了mito-miceΔ的肌肉病理。因此,严重线粒体疾病患者应尽量避免运动干预。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endurance swimming exacerbates mitochondrial myopathy in mice with high mtDNA deletions
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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