ArticleFrontiers in nutrition2022
MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats.
Article in Frontiers in nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection.Redox biology · 2026Article
- Mitochondrial-Derived Peptides as Therapeutics and Biomarkers for Combating Vascular Aging and Associated Cardiovascular Diseases.Current cardiology reviews · 2026Review
- Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-β signaling pathway.Frontiers in endocrinology · 2026Article
- MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.Frontiers in medicine · 2026Article
- Characterization of the Avian Mitochondrial-Derived Peptide MOTS-c and Its Potential Role as a Metabolic Regulator.Animals : an open access journal from MDPI · 2025Article
- MOTS-c: Magical Molecule for Diabetic Cardiomyopathy?Cardiovascular drugs and therapy · 2025Article
- MOTS-c mimics exercise to combat diabetic liver fibrosis by targeting Keap1-Nrf2-Smad2/3.Scientific reports · 2025Article
- Mitochondrial Dysfunction in the Development and Progression of Cardiometabolic Diseases: A Narrative Review.Journal of clinical medicine · 2025Review
- Circulating mitochondrial biomarkers in acute coronary syndrome.Frontiers in medicine · 2025Article
- Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.Biologics : targets & therapy · 2025Article
- Endogenous micropeptides as potential diagnostic biomarkers and therapeutic drugs.Frontiers in pharmacology · 2025Review
- Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart.Frontiers in physiology · 2025Article
- Mitochondrial-derived peptides in cardiovascular disease: Novel insights and therapeutic opportunities.Journal of advanced research · 2024Review
- MOTS-c regulates pancreatic alpha and beta cell functions in vitro.Histochemistry and cell biology · 2024Article
- The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.Scientific reports · 2023Article
- Early growth response-1: Key mediators of cell death and novel targets for cardiovascular disease therapy.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac structure remodeling and dysfunction are common complications of diabetes, often leading to serious cardiovascular events. MOTS-c, a mitochondria-derived peptide, regulates metabolic homeostasis by accelerating glucose uptake and improving insulin sensitivity. Plasma levels of MOTS-c are decreased in patients with diabetes. MOTS-c can improve vascular endothelial function, making it a novel therapeutic target for the cardiovascular complications of diabetes. We investigated the effects of MOTS-c on cardiac structure and function and analyzed transcriptomic characteristics in diabetic rats. Our results indicate that treatment with MOTS-c for 8-week repaired myocardial mitochondrial damage and preserved cardiac systolic and diastolic function. Transcriptomic analysis revealed that MOTS-c altered 47 disease causing genes. Functional enrichment analysis indicated MOTS-c attenuated diabetic heart disease involved apoptosis, immunoregulation, angiogenesis and fatty acid metabolism. Moreover, MOTS-c reduced myocardial apoptosis by downregulating CCN1 genes and thereby inhibiting the activation of ERK1/2 and the expression of its downstream EGR1 gene. Our findings identify potential therapeutic targets for the treatment of T2D and diabetic cardiomyopathy.
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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.