Study record

MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction

Li SH, Chen SQ, Lu T et al. · Life Sci · 2026

AnimalSeveralEvidence tier CAlso: Cell study (in vitro)

What this study reported

Measured lower serum MOTS-c in neonatal mice exposed to hyperoxia, which showed cardiac hypertrophy, fibrosis and dysfunction, and reported that administered MOTS-c was associated with attenuation of these changes. Reported that hyperoxia activated a KEAP1-PGAM5-AIFM1 oxeiptosis axis and that MOTS-c interacted with KEAP1, with KEAP1 overexpression abolishing the effect in cardiomyocytes.

Limitations

Male neonatal mice with group sizes not reported in the abstract; one immortalised rat cardiomyocyte line in vitro; only short-term outcomes assessed.

Study record

Annotated fields for this study
Study modelAnimal study (in vivo)
Substance studiedSeveralMore than one of these is central to the paper (common for reviews).
Speciesmouse, rat
System studiedHyperoxia-exposed neonatal C57BL/6 mice and hyperoxia-exposed H9C2 rat cardiomyocytes
PopulationNot reported
DesignControlled animal experiment with cell culture experiments
Sample size as reportednot reported
Control groupnormoxia-exposed and vehicle-treated hyperoxia-exposed animals and cells
Route (data field only)Not reported
Endpoints measuredserum MOTS-c content; cardiac hypertrophy and fibrosis; cardiac function; oxeiptosis and oxidative stress markers; KEAP1-PGAM5-AIFM1 axis
Pathways measuredOxidative stress · NRF2 / antioxidant response · Apoptosis
Research areasCardiovascular · Mitochondrial biology
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
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.