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Wang J et al. · Biochemical pharmacology ·
The study used db/db mice, a strain that develops diabetes and kidney damage, and treated them with MOTS-c at multiple doses. The paper reports that the urinary albumin-to-creatinine ratio was preserved in a dose-dependent manner, alongside less tubular injury, less lipid deposition, and fewer macrophages in the kidney. In kidney tissue and in HK-2 cells, MOTS-c lowered p16INK4A, γH2AX, and SA-β-gal activity, and changed levels of CPT1A and ADRP. The authors report that MOTS-c downregulated LARS1, which they describe as a negative regulator of lipophagy, and that this promoted LC3-mediated clearance of lipid droplets; overexpressing LARS1 in HK-2 cells reversed these effects. Co-administering the autophagy inhibitor 3-MA in db/db mice largely reversed the measured effects of MOTS-c, which the authors cite as evidence that lipophagy is involved.
Compounds