线粒体酸5减轻秀丽隐杆线虫与线粒体Ca2+超载相关的年龄相关神经肌肉功能障碍。

XinTong Wu, Miku Seida, Takaaki Abe, Atsushi Higashitani
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引用次数: 0

摘要

线粒体酸-5改善人类线粒体病成纤维细胞、秀丽隐杆线虫、杜氏肌营养不良和帕金森病模型的病理生理在这里,我们发现10 μM MA-5可以减轻秀丽隐杆线虫中与年龄相关的运动性能下降、肌肉线粒体丧失以及与线粒体Ca2+过载相关的多巴胺能神经元退化。这些发现表明,MA-5可能作为一种抗衰老剂,对后生动物的各种神经肌肉功能障碍起作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca<sup>2+</sup> overload in Caenorhabditis elegans.

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

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 μM 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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