ArticleInternational journal of molecular sciences2019
Mitochondrial-Derived Peptide MOTS-c Increases Adipose Thermogenic Activation to Promote Cold Adaptation.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- Deeply conserved and expressed small ORFs in the model beetle Tribolium castaneum.BMC biology · 2026Article
- Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.Inflammation and regeneration · 2026Article
- Octanoic acid treatment alleviates cold-induced depression-like behaviors via targeting the AKR1B1-PGF2α pathway.iScience · 2026Article
- Mitochondrial-derived microproteins in lung disease: insights and implications.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- MOTS‑c protects against placental injury via Nrf2 activation in hypoxia‑induced intrauterine growth restriction mice.International journal of molecular medicine · 2026Article
- Article
- MOTS-c regulates pancreatic alpha and beta cell functions in vitro.Histochemistry and cell biology · 2024Article
- MOTS-c is an effective target for treating cancer-induced bone pain through the induction of AMPK-mediated mitochondrial biogenesis.Acta biochimica et biophysica Sinica · 2024Article
- The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.Scientific reports · 2023Article
- Effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins.Biologia futura · 2023Article
- Inter-tissue communication of mitochondrial stress and metabolic health.Life metabolism · 2023Article
- Review
- Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.Journal of translational medicine · 2023Review
- MOTS-c Functionally Prevents Metabolic Disorders.Metabolites · 2023Review
- Mitochondrial polymorphism m.3017C>T of SHLP6 relates to heterothermy.Frontiers in physiology · 2023Article
- MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation.Frontiers in endocrinology · 2023Review
- O-GlcNAcylation of SIRT1 Protects against Cold Stress-Induced Skeletal Muscle Damage via Amelioration of Mitochondrial Homeostasis.International journal of molecular sciences · 2022Article
- Mitochondrial derived peptide MOTS-c prevents the development of heart failure under pressure overload conditions in mice.Journal of cellular and molecular medicine · 2022Article
- MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cold exposure stress causes hypothermia, cognitive impairment, liver injury, and cardiovascular diseases, thereby increasing morbidity and mortality. Paradoxically, cold acclimation is believed to confer metabolic improvement to allow individuals to adapt to cold, harsh conditions and to protect them from cold stress-induced diseases. However, the therapeutic strategy to enhance cold acclimation remains less studied. Here, we demonstrate that the mitochondrial-derived peptide MOTS-c efficiently promotes cold adaptation. Following cold exposure, the improvement of adipose non-shivering thermogenesis facilitated cold adaptation. MOTS-c, a newly identified peptide, is secreted by mitochondria. In this study, we observed that the level of MOTS-c in serum decreased after cold stress. MOTS-c treatment enhanced cold tolerance and reduced lipid trafficking to the liver. In addition, MOTS-c dramatically upregulated brown adipose tissue (BAT) thermogenic gene expression and increased white fat "browning". This effect might have been mediated by MOTS-c-activated phosphorylation of the ERK signaling pathway. The inhibition of ERK signaling disturbed the up-regulatory effect of MOTS-c on thermogenesis. In summary, our results indicate that MOTS-c treatment is a potential therapeutic strategy for defending against cold stress by increasing the adipose thermogenesis via the ERK pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.