MOTS-c cuts kidney injury in diabetic mice by downregulating LARS1
The mitochondrial-derived peptide preserved urinary albumin-to-creatinine ratio dose-dependently and reduced tubular senescence markers.
PR
By Priya Raman · Science Reporter
Oct 22 20:00 ETSource: Biochemical pharmacology
The wire
- 01In db/db mice, MOTS-c dose-dependently preserved urinary albumin-to-creatinine ratio, cut lipid deposition and lowered p16INK4A, γH2AX and SA-β-gal, acting through LARS1-mediated lipophagy.
- 02MOTS-c is a core longevity peptide on this beat, and readers track every mechanistic claim made for it.
- 03The work is in mice and HK-2 cells; autophagy inhibitor 3-MA reversed the effect, and no human data exist for diabetic nephropathy.
From the source
Read at pubmed.ncbi.nlm.nih.govMots-c attenuates diabetic nephropathy by downregulating LARS1 to promote lipophagy and suppress tubular senescence
Biochemical pharmacology · 2026 Oct 23 · Wang J, Luo S, Han Y et al.
Source URL https://pubmed.ncbi.nlm.nih.gov/42918312/
