• MSCs upregulate ARMC1 expression, which inhibits mitochondrial fission and reduces oxidative stress, thereby ameliorating renal fibrosis.
• ARMC1 overexpression enhances the anti-fibrotic effects of MSCs, suggesting ARMC1 as a potential therapeutic target.
• Combination therapy of MSCs with Mdivi-1 (Drp1 inhibitor) shows synergistic benefits in improving renal function and reducing fibrosis in a cisplatin-induced nephropathy model.
• The study provides evidence that targeting mitochondrial dynamics via ARMC1 could be a novel strategy for treating chronic kidney disease.