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

Abstract

Abstract The mitochondrial-homing drug MA-5 ameliorates the pathophysiology of human mitochondrial-disease fibroblasts and Caenorhabditis elegans DMD and PD disease models. Here, we found that MA-5 could suppress 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 suggest that MA-5 may act as an anti-aging agent against a wide range of neuromuscular dysfunctions in metazoan.