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.
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页数：5
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