ArticleCommunications biology2023
Extracellular vesicle-derived circCEBPZOS attenuates postmyocardial infarction remodeling by promoting angiogenesis via the miR-1178-3p/PDPK1 axis.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- 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
- HJournal of nanobiotechnology · 2026Article
- Circ_0041150 inhibits proliferation of pancreatic adenocarcinoma cells by regulating triglyceride accumulation via the miR-1178-3p/AADAC axis.Discover oncology · 2026Article
- Mechanisms and emerging research trends of angiogenesis promotion by small extracellular vesicles from different cellular sources in alleviating myocardial infarction injury.Frontiers in pharmacology · 2026Review
- Role of Exosomes in Cardiovascular Disease: A Key Regulator of Intercellular Communication in Cardiomyocytes.ACS omega · 2025Review
- Functions and application of circRNAs in vascular aging and aging-related vascular diseases.Journal of nanobiotechnology · 2025Review
- CircRNA Networks in CAD: Multi-Cellular Mechanisms and Clinical Potential.International journal of general medicine · 2025Review
- Extracellular vesicles in cardiovascular diseases: pathogenic mediators, diagnostic tools, and therapeutic vectors.Frontiers in cardiovascular medicine · 2025Review
- Circular RNAs in human diseases.MedComm · 2024Review
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Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging studies indicate that extracellular vesicles (EVs) and their inner circular RNAs (circRNAs), play key roles in the gene regulatory network and cardiovascular repair. However, our understanding of EV-derived circRNAs in cardiac remodeling after myocardial infarction (MI) remains limited. Here we show that the level of circCEBPZOS is downregulated in serum EVs of patients with the adverse cardiac remodeling compared with those without post-MI remodeling or normal subjects. Loss-of-function approaches in vitro establish that circCEBPZOS robustly promote angiogenesis. Overexpression of circCEBPZOS in mice attenuates MI-induced left ventricular dysfunction, accompanied by a larger functional capillary network at the border zone. Further exploration of the downstream target gene indicates that circCEBPZOS acts as a competing endogenous RNA by directly binding to miR-1178-3p and thereby inducing transcription of its target gene phosphoinositide-dependent kinase-1 (PDPK1). Together, our results reveal that circCEBPZOS attenuates detrimental post-MI remodeling via the miR-1178-3p/PDPK1 axis, which facilitates revascularization, ultimately improving the cardiac function.
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Registered trials
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