ArticleCardiovascular drugs and therapy2025
MOTS-c Peptide Attenuated Diabetic Cardiomyopathy in STZ-Induced Type 1 Diabetic Mouse Model.
Article in Cardiovascular drugs and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.Experimental physiology · 2026Article
- MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases.Journal of translational medicine · 2026Review
- MOTS‑c protects against placental injury via Nrf2 activation in hypoxia‑induced intrauterine growth restriction mice.International journal of molecular medicine · 2026Article
- FAP deficiency attenuates T2DM-associated HFpEF by suppressing the CaMKIIδ-Calcineurin A-NFATc2 signaling pathway.Clinical science (London, England : 1979) · 2025Article
- Crosstalk between perivascular adipose tissue and adipocyte-derived peptide in the pathogenesis of diabetic cardiomyopathy.Cardiovascular diabetology · 2025Review
- MOTS-c: Magical Molecule for Diabetic Cardiomyopathy?Cardiovascular drugs and therapy · 2025Article
- Enhancing Glucose Uptake as a Means to Protect the Heart During Cardiopulmonary Bypass or Ischemia-Reperfusion Injury.Cardiovascular drugs and 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
- A Backhanded Approach to Relieving Radial Artery Occlusion.Cardiovascular drugs and therapy · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic cardiomyopathy (DCM) pathogenesis is a common complication of diabetes, but effective treatments remain limited. Mitochondrial-derived peptide MOTS-c has shown therapeutic promise in animal models of various heart diseases, but its efficacy in DCM is unknown. This study investigates the effects of MOTS-c treatment in a mouse model of type 1 diabetes-induced DCM.
methodsType 1 diabetes (T1DM) was induced in mice by streptozotocin (STZ) injection. After diabetes establishment, the mice were randomly dividend into two groups treated with or without MOTS-c peptide, which was administered subcutaneously by osmotic pump for 12 weeks. At the end of the experiment, cardiac function, histology, and molecular changes were determined.
resultsThe results showed that diabetic mice exhibited significant cardiac dysfunction, dilatation, and adverse cardiac remodeling. MOTS-c treatment markedly ameliorated these diabetes-associated myocardial function and structure abnormalities. Additionally, MOTS-c reversed AMPK signaling deactivation and inhibited inflammation in the diabetic heart.
conclusionsOur data demonstrated a protective effect of MOTS-c against diabetic cardiomyopathy potentially by activating the AMPK pathway and inhibiting inflammation. These findings demonstrate the therapeutic efficacy of MOTS-c for diabetic cardiomyopathy and warrant further investigation into its clinical potential.
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