ArticleDiabetologia2021
Involvement of circHIPK3 in the pathogenesis of diabetic cardiomyopathy in mice.
Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Circular RNAs: Unlocking new avenues in cardiometabolic disease management.The Journal of physiology · 2026Review
- Review
- Circular RNAs as Biomarkers and Therapeutic Targets in Diabetic Cardiovascular Complications.Endocrinology, diabetes & metabolism · 2026Review
- Oxidative stress and ferroptosis in diabetic cardiomyopathy: mechanistic interplay and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025Review
- Non-Coding RNA in Type 2 Diabetes Cardio-Renal Complications and SGLT2 Inhibitor Response.International journal of molecular sciences · 2025Review
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- Epigenetic biomarkers predict macrovascular events in individuals with type 2 diabetes.Cell reports. Medicine · 2025Article
- Mechanistic exploration of hexokinase 2 and metabolism in diabetic cardiomyopathy.Molecular medicine reports · 2025Article
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Review
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- Functions and application of circRNAs in vascular aging and aging-related vascular diseases.Journal of nanobiotechnology · 2025Review
- CircHIPK3 targets DRP1 to mediate hydrogen peroxide-induced necroptosis of vascular smooth muscle cells and atherosclerotic vulnerable plaque formation.Journal of advanced research · 2025Article
- Circ-0001283 Aggravates Cardiac Hypertrophy by Targeting Myosin Light Chain 3 Protein.Research (Washington, D.C.) · 2025Article
- Mechanisms of circular RNAs in diabetic cardiomyopathy: biological characteristics and clinical prospects.Frontiers in genetics · 2025Review
- Circular RNAs in human diseases.MedComm · 2024Review
- Screening of differentially expressed RNAs and identifying a ceRNA axis during cadmium-induced oxidative damage in pancreatic β cells.Scientific reports · 2024Article
- Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisIn a mouse model of diabetic cardiomyopathy (DCM) the expression of the circular RNA circHIPK3 was found to be significantly increased. This study aimed to discover the molecular mechanisms linking circHIPK3 to the pathogenesis of DCM.
methodsThe diabetic mouse model was established by i.p. injection of streptozotocin, which led to the development of DCM. Echocardiographic measurements were used to evaluate cardiac structure and function, and histological staining was applied to detect myocardial fibrosis in mice. 5-Ethynyl-2'-deoxyuridine incorporation was performed to determine cell proliferation and RNA fluorescent in situ hybridisation was employed to examine circHIPK3 expression in cardiac fibroblasts. RNA immunoprecipitation and luciferase reporter assay were conducted to explore the pathological mechanism of circHIPK3 in myocardial fibrosis.
resultsKnockdown of circHIPK3 was found to attenuate myocardial fibrosis and enhance cardiac function in DCM mice. In addition, silencing of circHIPK3 could suppress proliferation of cardiac fibroblasts treated with angiotensin II. Furthermore, RNA immunoprecipitation and luciferase reporter assay revealed a circHIPK3-miR-29b-3p-Col1a1-Col3a1 regulatory network in the pathogenesis of myocardial fibrosis. CONCLUSIONS/
interpretationcircHIPK3 contributes to increased myocardial fibrosis during DCM by functioning as a competing endogenous RNA that upregulates Col1a1 and Col3a1 expression through suppressing miR-29b-3p.
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