ArticleMolecular and cellular biochemistry2017
MicroRNA-200c modulates DUSP-1 expression in diabetes-induced cardiac hypertrophy.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.
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Who cites it
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- A Systematic Study of Dysregulated MicroRNA in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2017Pooled it
- Dusp15 modulates mtHsp70 Thr116 phosphorylation state to preserve mito-UPR and attenuate cardiac dysfunction in diabetic cardiomyopathy.Cardiovascular diabetology · 2026Article
- Cardiovascular risk factors and modern therapeutic strategies in children and adolescents with type 1 diabetes to prevent future diabetic angiopathy in the era of innovative miRNAs biomarkers.Frontiers in endocrinology · 2025Review
- MicroRNA: unveiling novel mechanistic and theranostic pathways in diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
- Article
- Epigenetics of the Pathogenesis and Complications of Type 2 Diabetes Mellitus.TouchREVIEWS in endocrinology · 2023Review
- Deciphering the Role of miR-200c-3p in Type 1 Diabetes (Subclinical Cardiovascular Disease) and Its Correlation with Inflammation and Vascular Health.International journal of molecular sciences · 2022Article
- Adiponectin reduces apoptosis of diabetic cardiomyocytes by regulating miR-711/TLR4 axis.Diabetology & metabolic syndrome · 2022Article
- MiR-200c-3p Regulates DUSP1/MAPK Pathway in the Nonalcoholic Fatty Liver After Laparoscopic Sleeve Gastrectomy.Frontiers in endocrinology · 2022Article
- Whole patient knowledge modeling of COVID-19 symptomatology reveals common molecular mechanisms.Frontiers in molecular medicine · 2022Article
- Regulating Polyamine Metabolism by miRNAs in Diabetic Cardiomyopathy.Current diabetes reports · 2021Review
- Amniotic fluid microRNA profiles in twin-twin transfusion syndrome with and without severe recipient cardiomyopathy.American journal of obstetrics and gynecology · 2021Article
- miR-200c-3p Regulates Epitelial-to-Mesenchymal Transition in Epicardial Mesothelial Cells by Targeting Epicardial Follistatin-Related Protein 1.International journal of molecular sciences · 2021Article
- Research Progress on Epigenetics of Diabetic Cardiomyopathy in Type 2 Diabetes.Frontiers in cell and developmental biology · 2021Review
- Molecular Mechanisms and Epigenetic Regulation in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Dysregulation of circulating miRNAs promotes the pathogenesis of diabetes-induced cardiomyopathy.PloS one · 2021Article
- Sleeve Gastrectomy Ameliorates Diabetes-Induced Cardiac Hypertrophy Correlates With the MAPK Signaling Pathway.Frontiers in physiology · 2021Article
- Aging, MicroRNAs, and Heart Failure.Current problems in cardiology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein kinases (MAPKs) (ERK1/2, JNK, and p38) are upregulated in diabetic cardiomyopathy (DCM). Dual-specific phosphatase-1 (DUSP-1) has been reported to regulate the activity of MAPKs in cardiac hypertrophy; however, the role of DUSP-1 in regulating MAPKs activity in DCM is not known. MicroRNAs have been reported to regulate the expression of several genes in hypertrophied failing hearts. However, little is known about the microRNAs regulating DUSP-1 expression in diabetes-related cardiac hypertrophy. In the present study, we investigated the role of DUSP-1 and miR-200c in diabetes-induced cardiac hypertrophy. DCM was induced in Wistar rats by low-dose Streptozotocin high-fat diet for 12 weeks. Cardiac expression of ERK, p-38, JNK, DUSP-1, miR-200c, and hypertrophy markers (ANP and β-MHC) was studied in DCM in control rats and in high-glucose (HG)-treated rat neonatal cardiomyocytes. miR-200c inhibition was performed to validate DUSP-1 as target. A significant increase in phosphorylated ERK, p38, and JNK was observed in DCM model and in HG-treated cardiomyocytes (p < 0.05). Expression of DUSP-1 was significantly decreased in diabetes group and in HG-treated cardiomyocytes (p < 0.05). Increased expression of miR-200c was observed in DCM model and in HG-treated cardiomyocytes (p < 0.05). Inhibition of miR-200c induces the expression of the DUSP-1 causing decreased expression of phosphorylated ERK, p38, and JNK and attenuated cardiomyocyte hypertrophy in HG-treated cardiomyocytes. miR-200c plays a role in diabetes-associated cardiac hypertrophy by modulating expression of DUSP-1.
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