Study record

MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats

Wang M, Wang G, Pang X et al. · Front Nutr · 2022

AnimalMOTS-c administeredEvidence tier C

What this study reported

Reported that in diabetic rats administered MOTS-c, myocardial mitochondrial damage was reduced and cardiac systolic and diastolic function preserved. Reported that transcriptomic analysis identified 47 altered disease-associated genes with enrichment for apoptosis, immunoregulation, angiogenesis and fatty acid metabolism, and that lower myocardial apoptosis was accompanied by downregulation of CCN1, reduced ERK1/2 activation and lower EGR1 expression.

Limitations

Composition and size of the comparison groups are not described in the abstract; single rat diabetes model with sex not reported; mechanism inferred from transcriptomic enrichment and expression changes without pathway blockade; endpoints are surrogate cardiac and molecular measures.

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.
Speciesrat
System studiedDiabetic rats given MOTS-c, with cardiac imaging, myocardial histology and myocardial transcriptomics
PopulationNot reported
DesignControlled animal experiment with transcriptomic analysis
Sample size as reportedNot reported
Control groupNot reported
Route (data field only)Not reported
Endpoints measuredmyocardial mitochondrial ultrastructure; cardiac systolic and diastolic function; myocardial transcriptome; myocardial apoptosis; CCN1, ERK1/2 and EGR1 expression
Pathways measuredApoptosis · MAPK signalling · Lipid metabolism
Research areasCardiovascular · Metabolic
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
Limited
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.