Study record

Mitochondria-derived peptides in liver disease: Emerging regulators of hepatic metabolism and therapeutic targets

Thoudam T, Zeng G, Gao H et al. · Hepatol Commun · 2026

ReviewSeveralEvidence tier R

What this study reported

Reviewed published evidence on mitochondria-derived peptides in liver homeostasis and chronic liver disease, covering MOTS-c, humanin and small humanin-like peptides. Summarised reports that MOTS-c activates AMPK, regulates nuclear gene expression, suppresses fibrotic and inflammatory signalling and restores mitochondrial function in models of metabolic dysfunction-associated steatotic liver disease and fibrosis. Described proposed autocrine, paracrine and endocrine actions of these peptides.

Limitations

Narrative review without a stated search strategy or quality appraisal, summarising mainly cell and rodent models of liver disease, with MOTS-c one of several peptides discussed.

Study record

Annotated fields for this study
Study modelReview
Substance studiedSeveralMore than one of these is central to the paper (common for reviews).
SpeciesNot reported
System studiedPublished literature on mitochondria-derived peptides in liver homeostasis and chronic liver disease
PopulationNot reported
DesignNarrative review
Sample size as reportedNot reported
Control groupNot reported
Route (data field only)Not reported
Endpoints measuredreported roles of MOTS-c, humanin and SHLPs in hepatic metabolism; AMPK activation and nuclear gene regulation; fibrotic and inflammatory signalling in MASLD models; mitochondrial function, oxidative stress and apoptosis in hepatocytes
Pathways measuredAMPK signalling · Nuclear translocation · Inflammation · TGF-β / SMAD · Lipid metabolism · Apoptosis
Research areasLiver · Metabolic · Mitochondrial biology
Evidence tierR — Review (context, not evidence)
Publication typesJournal Article, Review

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
n/a
Sample size
n/a
Controls
n/a
Outcome validity
n/a
Support for its own conclusion
Weak

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.