Data edition of
Residue An evidence-graded reference for peptide science

MOTS-c research

What PubMed holds on MOTS-c, sorted by study design: the papers this site relies on, every clinical-trial publication PubMed tags, and the newest additions.

PubMed records
264
Trial publications
54 randomized
Reviews
59
Human-subject tagged
152
Animal-only
54
  • Clinical-trial publications 5
  • Reviews 59
  • Animal-only studies 54
  • Other (in vitro, chemistry, commentary, unindexed) 146
Figure 1. Composition of the MOTS-c literature by PubMed publication type and MeSH tags. Categories come from separate PubMed filters and can overlap; “animal-only” means tagged Animals and not Humans. Query: (MOTS-c[tiab] OR MOTSc[tiab]).
02651 2014: 1 records 2014 2015: 4 records 2015 2016: 3 records 2017: 4 records 2018: 10 records 2019: 19 records 2020: 16 records 2020 2021: 35 records 2022: 27 records 2023: 36 records 2024: 37 records 2025: 48 records 2025 2026: 51 records (year to date) 2026
Figure 2. PubMed records per publication year matching (MOTS-c[tiab] OR MOTSc[tiab]) — 264 in total; peak 51 in 2026. The 2026 bar is year-to-date (hatched). Volume of literature is not evidence of efficacy. Run this query on PubMed.

Studies this site relies on

Ordered by strength of design. Conclusions are quoted verbatim from each abstract as indexed by PubMed; read the full paper before relying on any of them.

  1. Primary study Nat Commun · 2021 PMID 33473109

    MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

    Reynolds JC, Lai RW, Woodhead JST, et al.

    In humans, exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation. Our data indicate that aging is regulated by genes encoded in both of our co-evolved mitochondrial and nuclear genomes.

  2. Primary study Am J Physiol Endocrinol Metab · 2021 PMID 33554779

    MOTS-c reduces myostatin and muscle atrophy signaling

    Kumagai H, Coelho AR, Wan J, et al.

    These results suggest that through inhibition of myostatin, MOTS-c could be a potential therapy for insulin resistance-induced skeletal muscle atrophy as well as other muscle wasting phenotypes including sarcopenia.NEW & NOTEWORTHY MOTS-c, a mitochondrial-derived peptide reduces high-fat-diet-induced muscle atrophy signaling by reducing …

  3. Primary study J Investig Med · 2018 PMID 29593067

    Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals

    Cataldo LR, Fernández-Verdejo R, Santos JL, et al.

    Such dependence seems altered when obesity settles. The implications of plasma MOTS-c for human metabolic homeostasis deserve future examination.

  4. Primary study Cell Metab · 2015 PMID 25738459

    The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

    Lee C, Zeng J, Drew BG, et al.

    MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome.

  5. Review Front Endocrinol (Lausanne) · 2023 PMID 36761202

    MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation

    Zheng Y, Wei Z, Wang T

    Throughout this paper, we discussed the discovery and physiological function of mitochondrial-derived polypeptide MOTS-c, and the application of MOTS-c in the treatment of various diseases, such as aging, cardiovascular disease, insulin resistance, and inflammation. To provide additional ideas for future research and development, we …

Clinical-trial publications in PubMed

5 records carry PubMed’s clinical-trial publication type. Tagging is done by NLM indexers and occasionally includes secondary analyses.

Newest records

The most recent PubMed additions for this query at the data-edition date, regardless of design.

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