Study record

Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway

Chen D, Zhou MH, Zhu WY et al. · Eur J Pharmacol · 2026

AnimalSeveralEvidence tier CAlso: Cell study (in vitro)

What this study reported

Measured lower MOTS-c content in neonatal mice with hyperoxia-induced bronchopulmonary dysplasia, and reported that administered MOTS-c was associated with less alveolar simplification, fewer pulmonary vascular abnormalities and less growth retardation. Reported that these effects, and the increases in endothelial cell viability and tube formation in human umbilical vein endothelial cells, were lost with an Nrf2 inhibitor or in Nrf2-deficient mice.

Limitations

Group sizes not reported in the abstract; male mice indexed in the record only; a single hyperoxia model with short-term endpoints and one endothelial cell type in vitro.

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, human
System studiedHyperoxia-exposed neonatal mice, including Nrf2-deficient mice, and hyperoxia-stimulated human umbilical vein endothelial cells
PopulationNot reported
DesignControlled animal experiment with cell culture experiments
Sample size as reportednot reported
Control groupvehicle-treated hyperoxia-exposed mice and normoxia controls
Route (data field only)other
Endpoints measuredalveolar simplification; pulmonary vascular development; growth retardation; inflammation and oxidative stress markers; endothelial cell viability and tube formation; Nrf2 pathway activity
Pathways measuredNRF2 / antioxidant response · Oxidative stress · Inflammation
Research areasLung · Mitochondrial biology · Inflammation & immunity
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.