Study record

Mitochondrial-derived peptide MOTS-c targets SLC7A11 to preserve spermatogenesis by suppressing ferroptosis

Liu S, Ru K, Shen YJ et al. · Free Radic Biol Med · 2026

AnimalSeveralEvidence tier CAlso: Human observationalAlso: Cell study (in vitro)

What this study reported

Measured lower serum MOTS-c in men with oligoasthenozoospermia, correlating with semen quality parameters. Reported that in a mechanical stress model in mice, administered MOTS-c was associated with less spermatogenic impairment, lower oxidative stress and less ferroptosis, and that SLC7A11 was identified as a target whose manipulation altered these effects in spermatogonia.

Limitations

Human component is cross-sectional with sample size not reported in the abstract; animal work uses one stress model; mechanistic claims rest largely on cell-level loss- and gain-of-function.

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).
Specieshuman, mouse
System studiedSerum from men with oligoasthenozoospermia; mouse microgravity-style mechanical stress model; spermatogonia with SLC7A11 manipulation
Populationmen with oligoasthenozoospermia (serum measurements)
DesignCase-control serum measurement with controlled animal and cell experiments
Sample size as reportednot reported
Control groupmen with normal semen parameters; untreated stressed mice and cells
Route (data field only)Not reported
Endpoints measuredserum MOTS-c levels; semen quality parameters; sperm concentration and seminiferous tubule architecture; oxidative stress and ferroptosis markers; SLC7A11 expression; spermatogonia proliferation
Pathways measuredOxidative stress · Apoptosis · Other
Research areasReproductive · 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
Human
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.