ArticleCellular & molecular biology letters2022
Therapeutic overexpression of miR-92a-2-5p ameliorated cardiomyocyte oxidative stress injury in the development of diabetic cardiomyopathy.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Long Noncoding RNA H19 Overexpression Inhibits High Glucose-Induced Oxidative Stress of Cardiomyocytes by Targeting MicroRNA-138-5p/MCU Axis: Implications for Diabetic Cardiomyopathy.Biochemical genetics · 2026Article
- Review
- GATA4-overexpressing BMSCs-derived exosome regulation of myocardial infarction in mice by key miRNA and apoptosis gene CLU.European journal of medical research · 2026Article
- Hsa_circ_0000313/miR-1224-3p/MKNK2 Axis Modulates CD4Mediators of inflammation · 2026Article
- Cardiovascular Dysfunction in Type 2 Diabetes: The Role of MicroRNAs.Handbook of experimental pharmacology · 2026Review
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- Canagliflozin protects cardiovascular function in type 2 diabetic coronary artery disease by regulating natriuretic peptide B.Journal of diabetes investigation · 2025Article
- Deciphering the role of crucial miRNAs involved in diabetic cardiomyopathy through a multiomics approach.Scientific reports · 2025Article
- Adipokines as Cardioprotective Factors: BAT Steps Up to the Plate.Biomedicines · 2025Review
- MicroRNA: unveiling novel mechanistic and theranostic pathways in diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- circLOC375190 promotes autophagy through modulation of the mTORC1/TFEB axis in acute ischemic stroke-induced neurological injury.Clinics (Sao Paulo, Brazil) · 2025Article
- Enhanced expression of miR-20a driven by nanog exacerbated the degradation of extracellular matrix in thoracic aortic dissection.Non-coding RNA research · 2024Article
- Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling.American journal of physiology. Heart and circulatory physiology · 2024Article
- MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
- Circulating MicroRNA as Biomarkers of Anthracycline-Induced Cardiotoxicity:JACC. CardioOncology · 2024Review
- Disrupted cardiac fibroblast BCAA catabolism contributes to diabetic cardiomyopathy via a periostin/NAP1L2/SIRT3 axis.Cellular & molecular biology letters · 2023Article
- An integrative review of nonobvious puzzles of cellular and molecular cardiooncology.Cellular & molecular biology letters · 2023Review
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDiabetic cardiomyopathy (DCM) results from pathological changes in cardiac structure and function caused by diabetes. Excessive oxidative stress is an important feature of DCM pathogenesis. MicroRNAs (miRNAs) are key regulators of oxidative stress in the cardiovascular system. In the present study, we screened for the expression of oxidative stress-responsive miRNAs in the development of DCM. Furthermore, we aimed to explore the mechanism and therapeutic potential of miR-92a-2-5p in preventing diabetes-induced myocardial damage.
methodsAn experimental type 2 diabetic (T2DM) rat model was induced using a high-fat diet and low-dose streptozotocin (30 mg/kg). Oxidative stress injury in cardiomyocytes was induced by high glucose (33 mmol/L). Oxidative stress-responsive miRNAs were screened by quantitative real-time PCR. Intervention with miR-92a-2-5p was accomplished by tail vein injection of agomiR in vivo or adenovirus transfection in vitro.
resultsThe expression of miR-92a-2-5p in the heart tissues was significantly decreased in the T2DM group. Decreased miR-92a-2-5p expression was also detected in high glucose-stimulated cardiomyocytes. Overexpression of miR-92a-2-5p attenuated cardiomyocyte oxidative stress injury, as demonstrated by increased glutathione level, and reduced reactive oxygen species accumulation, malondialdehyde and apoptosis levels. MAPK interacting serine/threonine kinase 2 (MKNK2) was verified as a novel target of miR-92a-2-5p. Overexpression of miR-92a-2-5p in cardiomyocytes significantly inhibited MKNK2 expression, leading to decreased phosphorylation of p38-MAPK signaling, which, in turn, ameliorated cardiomyocyte oxidative stress injury. Additionally, diabetes-induced myocardial damage was significantly alleviated by the injection of miR-92a-2-5p agomiR, which manifested as a significant improvement in myocardial remodeling and function.
conclusionsmiR-92a-2-5p plays an important role in cardiac oxidative stress, and may serve as a therapeutic target in DCM.
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