Review of evidence for MOTS-c as a potential anti-pulmonary fibrosis therapy, examining how MOTS-c addresses the aging, oxidative stress, metabolic dysfunction, and mitochondrial dysfunction that contribute to idiopathic pulmonary fibrosis pathogenesis, with discussion of MOTS-c's anti-fibrotic mechanisms in lung tissue. Positions MOTS-c as an IPF therapeutic candidate. Provides the first dedicated synthesis of MOTS-c's potential in pulmonary fibrosis—a progressive fatal lung disease with limited treatment options—establishing the mechanistic rationale for investigating mitochondrial peptide supplementation in a disease where mitochondrial dysfunction and oxidative stress drive fibroblast activation.
Zhang, Zewei; Chen, Dongmei; Du, Kaili; Huang, Yaping; Li, Xingzhe; Li, Quwen; Lv, Xiaoting