Research summary
Research HubMOTS-c
Clinical — 10 studies
MOTS-c is a mitochondrially encoded peptide, measured in human serum studies and tested in cell and animal models of organ injury. Most recent papers examine Nrf2 and AMPK signalling in lung, joint, disc and liver models.
Updated
Being studied for
- Circulating levels in human cohorts
- Lung ischaemia-reperfusion models
- Osteoarthritis and disc degeneration
- Hepatitis B infection models
- Exercise and cardiac adaptation
What the research shows
All ten cited papers are recent, published between 2023 and 2025. Two measured circulating MOTS-c in people without giving it: one in women with preeclampsia, the other in adults with and without obesity. The remaining eight are preclinical and gave or expressed the peptide in models of allergic asthma, lung ischaemia-reperfusion, lung injury after cardiopulmonary bypass, osteoarthritis, intervertebral disc degeneration, diabetic liver fibrosis and hepatitis B infection, plus a rat study that set it beside aerobic exercise.
Neither human study found a difference between the groups compared. Serum levels did not differ in preeclampsia and were similar in people with obesity and those of normal weight, with age and insulin resistance emerging as determinants. The preclinical papers reported less injury or degeneration by several mechanisms: reduced airway epithelial apoptosis via Nrf2 in asthma, activation of nuclear antioxidant defences through ROS-CK2A-MYH9 signalling after lung ischaemia-reperfusion, greater glycolysis and suppressed ferroptosis via AMPK-HIF-1α after bypass, slower cartilage degeneration via Nrf2 in osteoarthritis, and anti-degenerative effects associated with AMPK/SIRT1 signalling in disc-derived stem cells carried in a peptide hydrogel. In liver fibrosis experiments it lowered reactive oxygen species, raised Keap1-Nrf2 pathway expression and reduced TGF-β1/Smad expression. In hepatitis B it was linked to mitochondrial remodelling and antiviral activity. In rats, both MOTS-c and aerobic training increased heart weight and thickened myocardial fibres.
The picture is broad but thin. Each disease model rests on one study, most of them from 2025, and the pathways named differ from paper to paper, although Nrf2 appears in three. No cited study gave MOTS-c to people, and the preeclampsia authors called for large-scale research to clarify whether it has a role as a biomarker. Several papers present MOTS-c as a possible biomarker or therapeutic agent; those are hypotheses drawn from animal and cell work, not findings in patients.
Published Research
Evidence profile
Preclinical, with limited uncontrolled human reports
10 cited publications
Findings below belong to the studies that reported them. They describe the material and conditions those authors used, not this product, and not an outcome to expect.
Additional indexed literature (10)
- Clinical · Mechanistic studyMOTS-C levels ın ındividuals with and without obesity and ıts association with ınflammation, insulin resistance and endothelial dysfunction
Ozkaya DY et al. · Archives of endocrinology and metabolism · 2025 · PMID 41004666
- Observational · Mechanistic studySerum MOTS-c levels remain unchanged in patients with preeclampsia
Tok A et al. · Ginekologia polska · 2023 · PMID 39469962
- Preclinical · Mechanistic studyMOTS-c attenuates airway barrier dysfunction in allergic asthma by inhibiting epithelial apoptosis via Nrf2 pathway
Zhang W et al. · International immunopharmacology · 2025 · PMID 40472776
- Preclinical · Mechanistic studyMOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration
Lin Y et al. · Materials today. Bio · 2025 · PMID 40510834
- Preclinical · Mechanistic studyMOTS-c attenuates lung ischemia-reperfusion injury via MYH9-Dependent nuclear translocation and transcriptional activation of antioxidant genes
Li X et al. · Redox biology · 2025 · PMID 40403491
- Preclinical · Mechanistic studyMOTS-c attenuates mitochondrial dysfunction induces pyroptosis and cartilage degradation in osteoarthritis via an Nrf2-Dependent Mechanism
Li K et al. · Free radical biology & medicine · 2025 · PMID 41043625
- Preclinical · Mechanistic studyMOTS-c Promotes Glycolysis via AMPK-HIF-1α-PFKFB3 Pathway to Ameliorate Cardiopulmonary Bypass-induced Lung Injury
Shen Z et al. · American journal of respiratory cell and molecular biology · 2025 · PMID 40035775
- Preclinical · Mechanistic studyMOTS-c mimics exercise to combat diabetic liver fibrosis by targeting Keap1-Nrf2-Smad2/3
Chen F et al. · Scientific reports · 2025 · PMID 40425777
- Preclinical · Mechanistic studyNovel function of MOTS-c in mitochondrial remodelling contributes to its antiviral role during HBV infection
Lin C et al. · Gut · 2024 · PMID 37788894
- Preclinical · Mechanistic studyMOTS-c and aerobic exercise induce cardiac physiological adaptation via NRG1/ErbB4/CEBPβ modification in rats
Yuan J et al. · Life sciences · 2023 · PMID 36584915
Published studies summarised here concern the specific investigational or pharmaceutical materials and study conditions described by their authors. Their findings are not performance claims for Cobalt Peptides material. Citations verified against PubMed on 2026-09-29.
The studies summarised here are research reports; nothing on this page is guidance on use in people or animals.
Notice
All information on this page is provided strictly for laboratory research and educational purposes only.