Study record

Mitochondrial-derived microproteins in cancer and neurodegeneration: A new era of cross-disease mechanistic insights

Hu S, Hu C, Tong M · Pathol Res Pract · 2026

ReviewSeveralEvidence tier R

What this study reported

Reviewed reported signalling pathways of mitochondrial-derived microproteins, including the MOTS-c-AMPK/NRF2-LARS1/mTORC1 axis, alongside humanin, SHLPs and SHMOOSE. Summarised how these pathways have been linked to apoptosis, nutrient sensing, redox balance and mito-nuclear communication in cancer and neurodegeneration literature. Described methodological advances such as mitoribosome profiling, proteogenomics and mitochondrial base editing.

Limitations

Narrative review with no stated search strategy or appraisal of source study quality, covering MOTS-c as one of several microproteins, and much of the synthesised evidence comes from cell and animal work.

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 mitochondrial-derived microproteins in cancer and neurodegeneration
PopulationNot reported
DesignNarrative review
Sample size as reportedNot reported
Control groupNot reported
Route (data field only)Not reported
Endpoints measuredreported signalling architectures of humanin, MOTS-c, SHLPs and SHMOOSE; MOTS-c-AMPK/NRF2-LARS1/mTORC1 signalling; disease-specific outcomes in cancer and neurodegeneration; discovery methods for mitochondrial-derived microproteins
Pathways measuredAMPK signalling · NRF2 / antioxidant response · AKT / mTOR / FOXO · Apoptosis · Oxidative stress
Research areasCancer · Nervous system · 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
Indirect
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.