Study record

Mots-c attenuates diabetic nephropathy by downregulating LARS1 to promote lipophagy and suppress tubular senescence

Wang J, Luo S, Han Y et al. · Biochem Pharmacol · 2026

AnimalMOTS-c administeredEvidence tier CAlso: Cell study (in vitro)

What this study reported

Reported that administered MOTS-c was associated with preserved urinary albumin-to-creatinine ratio, less tubular injury, less lipid deposition and less macrophage accumulation in db/db mice. Reported lower p16, gammaH2AX and SA-beta-gal signal and lower LARS1 with increased LC3-mediated lipid droplet clearance, with LARS1 overexpression in HK-2 cells and an autophagy inhibitor in mice reversing these changes.

Limitations

Group sizes and sex not reported in the abstract; a single genetic diabetes model and one human tubular cell line; mechanism relies on a non-selective autophagy inhibitor.

Study record

Annotated fields for this study
Study modelAnimal study (in vivo)
Substance studiedMOTS-c administeredSynthetic MOTS-c was given to cells, animals or people.
Speciesmouse, human
System studieddb/db mice with diabetic nephropathy and HK-2 human proximal tubular cells with LARS1 overexpression
PopulationNot reported
DesignControlled animal experiment with cell culture experiments and transcriptomics
Sample size as reportednot reported
Control groupuntreated db/db mice; cells without LARS1 overexpression
Route (data field only)Not reported
Endpoints measuredurinary albumin-to-creatinine ratio; tubular injury and lipid deposition; macrophage accumulation; senescence markers (p16, gammaH2AX, SA-beta-gal); LARS1 expression and lipophagy markers
Pathways measuredAutophagy / mitophagy · Lipid metabolism · Inflammation
Research areasKidney · Metabolic · Aging
Evidence tierC — Animal in vivo
Publication typesJournal Article

Appraisal

Each dimension is recorded separately and never combined into a single score. A study can be well controlled and still tell you little about people.

Relevance to MOTS-c
Direct
Model applicability
Mammalian
Sample size
Not reported
Controls
Appropriate
Outcome validity
Validated biomarker
Support for its own conclusion
Moderate

Provenance

  • Bibliographic fields retrieved from PubMed E-utilities efetch (title, journal, date, authors, DOI) on 2026-11-11.
  • Annotated from the published abstract.
  • Editorial review: approved (2026-11-11).
  • Classification follows the site methodology; the record describes the study, not what MOTS-c does in people.