Study record

The role of FPR2-mediated ferroptosis in formyl peptide-induced acute lung injury against endothelial barrier damage and protective effect of the mitochondria-derived peptide MOTS-c

Wen Z, Fan J, Zhan F et al. · Int Immunopharmacol · 2024

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

What this study reported

Reported that fMLP promoted ferroptosis and endothelial barrier disruption in rat lungs and in human pulmonary microvascular endothelial cells, and that MOTS-c was associated with less ferroptosis and with lower inflammatory and oxidative stress markers through Nrf2 and MAPK signalling.

Limitations

Single acute injury model with group sizes and blinding not reported; the mechanism rests on FPR2 knockdown and inhibitors in one endothelial cell line; rodent and cell findings do not transfer to people.

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, human
System studiedRats with fMLP-induced acute lung injury and human pulmonary microvascular endothelial cells
PopulationNot reported
DesignControlled animal experiment with cell culture experiments
Sample size as reportedNot reported
Control groupfMLP-exposed rats and cells not given MOTS-c
Route (data field only)Not reported
Endpoints measuredlung histopathology; inflammatory and oxidative stress markers; ferroptosis-related proteins; endothelial barrier proteins; Nrf2 and MAPK signalling
Pathways measuredNRF2 / antioxidant response · MAPK signalling · Oxidative stress · Inflammation
Research areasLung · 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.