ArticleCell death and differentiation2022
The circRNA CNEACR regulates necroptosis of cardiomyocytes through Foxa2 suppression.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
- The emerging roles of small nucleolar RNAs, piwi-interacting RNAs, tRNA-derived small RNAs, and circular RNAs in the regulation of cardiac hypertrophy, ischemic heart disease, and heart failure.Genes & diseases · 2026Review
- Monotropein mitigates atherosclerotic plaque vulnerability through circ_0140736/miR-495/SIRPα-mediated efferocytosis.iScience · 2026Article
- Downregulation of circ_0001112 Enhances Myocardial Infarction Through Regulation of miR-324-5p/CDK6 Axis.Journal of biochemical and molecular toxicology · 2026Article
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- CircRNA-regulated programmed cell death networks in cardiomyocytes: Molecular crosstalk and therapeutic translation.Non-coding RNA research · 2026Review
- Circular RNA as emerging precision therapeutics: from RNA regulation to peptide translation.Precision clinical medicine · 2026Review
- Epigenetic Regulation of Regulated Cell Death in Aging-Related Diseases: Clinical Perspectives.Aging and disease · 2025Article
- The multiplex crosstalk between non-coding RNAs, programmed cell death and related mechanisms: a dynamic duo in hematological malignancies.Cancer cell international · 2025Review
- Circular RNAs in Cardiovascular Physiopathology: From Molecular Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential.Apoptosis : an international journal on programmed cell death · 2025Review
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Noncoding RNAs in myocardial ischemia/reperfusion injury and repair.Current opinion in physiology · 2025Article
- Circular RNAs modulate cell death in cardiovascular diseases.Cell death discovery · 2025Review
- Article
- Epigenetic Regulation of Chromatin Functions by MicroRNAs and Long Noncoding RNAs and Implications in Human Diseases.Biomedicines · 2025Review
- Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.Cell death discovery · 2025Review
- Inhibition of circALPK2 enhances proliferation and therapeutic potential of human pluripotent stem cell-derived cardiomyocytes in myocardial infarction.Stem cell research & therapy · 2025Article
- Scaffolding Activities of Pseudodeacetylase HDAC7.ACS chemical biology · 2025Review
- CircRNA Networks in CAD: Multi-Cellular Mechanisms and Clinical Potential.International journal of general medicine · 2025Review
- CircFndc3b Mediates Exercise-Induced Neuroprotection by Mitigating Microglial/Macrophage Pyroptosis via the ENO1/KLF2 Axis in Stroke Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circular RNAs (circRNAs) are differentially expressed in various cardiovascular disease including myocardial ischemia-reperfusion (I/R) injury. However, their functional impact on cardiomyocyte cell death, in particular, in necrotic forms of death remains elusive. In this study, we found that the level of mmu_circ_000338, a cardiac- necroptosis-associated circRNA (CNEACR), was reduced in hypoxia-reoxygenation (H/R) exposed cardiomyocytes and I/R-injured mice hearts. The enforced expression of CNEACR attenuated the necrotic form of cardiomyocyte death caused by H/R and suppressed of myocardial necrosis in I/R injured mouse heart, which was accompanied by a marked reduction of myocardial infarction size and improved cardiac function. Mechanistically, CNEACR directly binds to histone deacetylase (HDAC7) in the cytoplasm and interferes its nuclear entry. This leads to attenuation of HDAC7-dependent suppression of forkhead box protein A2 (Foxa2) transcription, which can repress receptor-interacting protein kinase 3 (Ripk3) gene by binding to its promoter region. In addition, CNEACR-mediated upregulation of FOXA2 inhibited RIPK3-dependent necrotic/necroptotic death of cardiomyocytes. Our study reveals that circRNAs such as CNEACR can regulate the cardiomyocyte necroptosis associated activity of HDACs, promotes cell survival and improves cardiac function in I/R-injured heart. Hence, the CNEACR/HDAC7/Foxa2/ RIPK3 axis could be an efficient target for alleviating myocardial damage caused by necroptotic death in ischemia heart diseases.
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