ArticleJournal of cellular and molecular medicine2020
Inhibition of miR-21 alleviated cardiac perivascular fibrosis via repressing EndMT in T1DM.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Beyond EMT: Mesenchymal drift as an emerging driver of stromal-immune reprogramming in prostate cancer.iScience · 2026Review
- Endothelial-to-Mesenchymal Transition in Post-Myocardial Infarction Fibrosis: A Maladaptive but Targetable Pathway.EJIFCC · 2026Review
- Ginsenoside Rb1 Mitigates Myocardial Fibrosis Through Inhibiting Exosomal-Derived miRNA-21-Associated Inflammation and Cardiac Signaling.Cardiovascular therapeutics · 2026Article
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Endothelin as a Treatment Target in Cardiovascular Diseases: A Recent Step Forward.Reviews in cardiovascular medicine · 2025Review
- Review
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- Interplay Between TGF-β Signaling and MicroRNA in Diabetic Cardiomyopathy.Cardiovascular drugs and therapy · 2025Review
- Lipoxin ACardiovascular diabetology · 2024Article
- Paediatrics congenital heart disease is associated with plasma miRNAs.Pediatric research · 2024Article
- Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue.International journal of molecular sciences · 2024Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
- Unraveling the Cardiac Matrix: From Diabetes to Heart Failure, Exploring Pathways and Potential Medications.Biomedicines · 2024Review
- SirT7-mediated transcription of fascin in hyperglycemic glomerular endothelial cells contributes to EndMT in diabetic nephropathy.Acta biochimica et biophysica Sinica · 2024Article
- Non-coding RNAs: targets for Chinese herbal medicine in treating myocardial fibrosis.Frontiers in pharmacology · 2024Review
- Study on the Mechanism of Estrogen Regulating Endometrial Fibrosis After Mechanical Injury Via MIR-21-5P/PPARΑ/FAO Axis.Current molecular medicine · 2024Article
- Experimental Models to Study Endothelial to Mesenchymal Transition in Myocardial Fibrosis and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In type 1 and type 2 diabetes mellitus, increased cardiac fibrosis, stiffness and associated diastolic dysfunction may be the earliest pathological phenomena in diabetic cardiomyopathy. Endothelial-mesenchymal transition (EndMT) in endothelia cells (ECs) is a critical cellular phenomenon that increases cardiac fibroblasts (CFs) and cardiac fibrosis in diabetic hearts. The purpose of this paper is to explore the molecular mechanism of miR-21 regulating EndMT and cardiac perivascular fibrosis in diabetic cardiomyopathy. In vivo, hyperglycaemia up-regulated the mRNA level of miR-21, aggravated cardiac dysfunction and collagen deposition. The condition was recovered by inhibition of miR-21 following with improving cardiac function and decreasing collagen deposition. miR-21 inhibition decreased cardiac perivascular fibrosis by suppressing EndMT and up-regulating SMAD7 whereas activating p-SMAD2 and p-SMAD3. In vitro, high glucose (HG) up-regulated miR-21 and induced EndMT in ECs, which was decreased by inhibition of miR-21. A highly conserved binding site of NF-κB located in miR-21 5'-UTR was identified. In ECs, SMAD7 is directly regulated by miR-21. In conclusion, the pathway of NF-κB/miR-21/SMAD7 regulated the process of EndMT in T1DM, in diabetic cardiomyopathy, which may be regarded as a potential clinical therapeutic target for cardiac perivascular fibrosis.
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