Study record

Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells

Xing L, Lu B, Zhu X et al. · Inflamm Regen · 2026

CellsSeveralEvidence tier DAlso: Animal study (in vivo)

What this study reported

Measured lower basal MOTS-c expression in mesenchymal stromal cells from donors with obesity, and reported that MOTS-c co-incubation restored intracellular levels and activated AMPK but reduced proliferation and increased p16, p21 and TNF-alpha expression. Reported that MOTS-c-pretreated cells failed to improve renal perfusion, fibrosis or tubular injury in mice with renal artery stenosis, and that pretreatment also blunted the effect of lean-donor cells.

Limitations

Small donor numbers per group; a single cell type and one murine renal stenosis model; effects assessed after in-culture exposure rather than systemic administration.

Study record

Annotated fields for this study
Study modelCell study (in vitro)
Substance studiedSeveralMore than one of these is central to the paper (common for reviews).
Specieshuman, mouse
System studiedAdipose-derived mesenchymal stromal cells from donors with obesity and lean donors; MOTS-c-pretreated cells delivered to stenotic mouse kidneys
PopulationNot reported
DesignCell culture experiments with a controlled animal model
Sample size as reported6 donors per group
Control groupuntreated obese and lean donor cells; untreated stenotic kidney animals
Route (data field only)in-culture
Endpoints measuredMSC proliferation; senescence gene expression (p16, p21); TNF-alpha and antioxidant gene expression; AMPK signalling; renal perfusion, fibrosis and tubular injury
Pathways measuredAMPK signalling · Inflammation · Oxidative stress
Research areasKidney · Metabolic · Aging · Mitochondrial biology
Evidence tierD — Cell, tissue or analytical
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
Small
Controls
Appropriate
Outcome validity
Surrogate
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.