Study record

LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection

Zhang YL, Huang G, Li SP et al. · Redox Biol · 2026

AnimalMOTS-c analogue or derivativeEvidence tier CAlso: Cell study (in vitro)Also: Analytical / methods

What this study reported

Reported that substituting arginine 13 with alanine increased the peptide's hydrophobicity and cellular uptake, and that uptake of R13A-MOTS-c depended on LAT1 in lung epithelial cells. Reported that in irradiated mice the analogue was associated with less pulmonary inflammation, oxidative stress and mitochondrial dysfunction, with effects lost under LAT1 or Nrf2 inhibition or Nrf2 knockout.

Limitations

Findings concern an engineered analogue rather than native MOTS-c; group sizes not reported in the abstract; a single irradiation model and one lung epithelial cell line.

Study record

Annotated fields for this study
Study modelAnimal study (in vivo)
Substance studiedMOTS-c analogue or derivativeA modified peptide or drug derived from MOTS-c, which is not the same molecule.
Speciesmouse
System studiedEngineered R13A-MOTS-c in MLE-12 lung epithelial cells and in thoracically irradiated C57BL/6 and Nrf2-knockout mice
PopulationNot reported
DesignPeptide engineering with cell culture and controlled animal experiments
Sample size as reportednot reported
Control groupvehicle-treated irradiated mice; wild-type MOTS-c and untreated cells
Route (data field only)intraperitoneal
Endpoints measuredcellular uptake and LAT1 dependence; inflammatory markers; oxidative damage; mitochondrial function; Nrf2 nuclear translocation and target genes
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
Indirect
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.