Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca2+ overload in Caenorhabditis elegans

被引：0

作者：

Wu, XinTong ^{[1
]}

Seida, Miku ^{[1
]}

Abe, Takaaki ^{[2
,3
]}

Higashitani, Atsushi ^{[1
]}

机构：

[1] Tohoku Univ, Grad Sch Life Sci, Sendai 9808577, Japan

[2] Tohoku Univ, Div Med Sci, Grad Sch Biomed Engn, Sendai 9800872, Japan

[3] Tohoku Univ, Dept Clin Biol & Hormonal Regulat, Grad Sch Med, Sendai 9800872, Japan

来源：

NPJ AGING | 2023年 / 9卷 / 01期

基金：

美国国家卫生研究院;

关键词：

CRISTAE; MORPHOLOGY; SURVIVAL; CALCIUM; MA-5;

D O I：

10.1038/s41514-023-00116-2

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Mitochonic acid-5 ameliorates the pathophysiology of human mitochondrial-disease fibroblasts and Caenorhabditis elegans Duchenne muscular dystrophy and Parkinson's disease models. Here, we found that 10 & mu;M MA-5 attenuates the age-related decline in motor performance, loss of muscle mitochondria, and degeneration of dopaminergic neurons associated with mitochondrial Ca2+ overload in C. elegans. These findings suggest that MA-5 may act as an anti-aging agent against a wide range of neuromuscular dysfunctions in metazoans.

引用

页数：5

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