ArticlePeerJ2023
miR-200a-3p overexpression alleviates diabetic cardiomyopathy injury in mice by regulating autophagy through the FOXO3/Mst1/Sirt3/AMPK axis.
Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- The expression profiles and roles of microRNAs in cardiac glucose metabolism.Frontiers in endocrinology · 2025Pooled it
- Targeting SIRT3 in Diabetic Cardiomyopathy: Mechanism-Based Therapeutic Strategies.Cardiovascular drugs and therapy · 2026Review
- MiR-200a-3p protects against myocardial ischemia-reperfusion injury via KEAP1-NRF2 signaling.Frontiers in physiology · 2026Article
- Targeting SIRT3 to Ameliorate Diabetic Cardiomyopathy: Progress in Mechanistic Research and Prospects for Clinical Translation.Journal of diabetes · 2025Review
- The crosstalk between MicroRNAs and sirtuins: a bit unexpected therapeutic target for cardiovascular diseases.European journal of medical research · 2025Review
- Emerging Biomarkers and Nanobiosensing Strategies in Diabetes.Biosensors · 2025Review
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- Inhibiting miR-200a-3p Increases Sirtuin 1 and Mitigates Kidney Injury in a Tubular Cell Model of Diabetes and Hypertension-Related Renal Damage.Biomolecules · 2025Article
- Muscle-Derived miR-200a-3p Through Light-Intensity Exercise May Contribute to Improve Memory Dysfunction in Type 2 Diabetic Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Non-coding RNAs affecting NLRP3 inflammasome pathway in diabetic cardiomyopathy: a comprehensive review of potential therapeutic options.Journal of translational medicine · 2025Review
- Therapeutic potential of finerenone for diabetic cardiomyopathy: focus on the mechanisms.Diabetology & metabolic syndrome · 2024Review
- Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue.International journal of molecular sciences · 2024Review
- Exploring Sirtuins: New Frontiers in Managing Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- The modulation of immune cell death in connection to microRNAs and natural products.Frontiers in immunology · 2024Review
- miR-200a-3p Targets and Downregulates CDC25B Expression to Inhibit the Progression of Hepatocellular Carcinoma.BioFactors (Oxford, England)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Hyperglycemia and insulin resistance or deficiency are characteristic features of diabetes. Diabetes is accompanied by cardiomyocyte hypertrophy, fibrosis and ventricular remodeling, and eventually heart failure. In this study, we established a diabetic cardiomyopathy (DCM) mouse model to explore the role and mechanism of miR-200a-3p in DCM. Methods: We used db/db mice to simulate the animal model of DCM and the expression of miR-200a-3p was then examined by RT-qPCR. Tail vein injection of mice was done with rAAV-miR-200a-3p for 8 weeks, and cardiac function was assessed by cardiac ultrasound. The levels of myocardial tissue injury, fibrosis, inflammation, apoptosis and autophagy in mice were detected by histological staining, TUNEL and other molecular biological experiments. Results: miR-200a-3p expression levels were significantly decreased in the myocardium of DCM mice. Diabetic mice developed cardiac dysfunction and presented pathological changes such as myocardial injury, myocardial interstitial fibrosis, cardiomyocyte apoptosis, autophagy, and inflammation. Overexpression of miR-200a-3p expression significantly ameliorated diabetes induced-cardiac dysfunction and myocardial injury, myocardial interstitial fibrosis, cardiomyocyte apoptosis, and inflammation, and enhanced autophagy. Mechanistically, miR-200a-3p interacted with FOXO3 to promote Mst1 expression and reduce Sirt3 and p-AMPK expression. Conclusion: In type 2 diabetes, increased miR-200a-3p expression enhanced autophagy and participated in the pathogenic process of cardiomyopathy throug7 Mst1/Sirt3/AMPK axis regulation by its target gene FOXO3. This conclusion provides clues for the search of new gene targeted therapeutic approaches for diabetic cardiomyopathy.
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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.