ArticleOxidative medicine and cellular longevity2022
Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 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
- Brain-derived extracellular vesicles potentially mediate crosstalk with peripheral organs in neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
- Circular RNAs in human diseases.MedComm · 2024Review
- Review
- The immune regulatory role of exosomal miRNAs and their clinical application potential in heart failure.Frontiers in immunology · 2024Review
- CircRNA-mediated regulation of cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- Exosomes as Vehicles for Noncoding RNA in Modulating Inflammation: A Promising Regulatory Approach for Ischemic Stroke and Myocardial Infarction.Journal of inflammation research · 2024Review
- LncRNA/CircRNA-miRNA-mRNA Axis in Atherosclerotic Inflammation: Research Progress.Current pharmaceutical biotechnology · 2024Review
- ITGB1 alleviates osteoarthritis by inhibiting cartilage inflammation and apoptosis via activating cAMP pathway.Journal of orthopaedic surgery and research · 2023Article
- Circular RNAs Variously Participate in Coronary Atherogenesis.Current issues in molecular biology · 2023Review
- Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?Journal of clinical medicine · 2023Review
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Exosomes as a delivery tool of exercise-induced beneficial factors for the prevention and treatment of cardiovascular disease: a systematic review and meta-analysis.Frontiers in physiology · 2023Review
- Immune cells-derived exosomes function as a double-edged sword: role in disease progression and their therapeutic applications.Biomarker research · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction (AMI) is a complication of atherosclerosis-related cardiovascular illness that is caused by prolonged ischemia. Circular RNAs (circRNAs) are concentrated in extracellular vesicles (EVs) and have been linked to cardiovascular disease. However, additional research is needed into the expression and function of circRNAs in AMI. In this study, circITGB1 (has_circRNA_0018146), derived from exon 1 of the ITGB1 gene localized on chromosome 10, was shown to be considerably increased in plasma from patients with AMI compared to healthy controls, as demonstrated by the comparison of EV-circRNA expression patterns. Using a luciferase screening assay and a biotin-labeled circITGB1 probe to identify microRNA(s) complementary to circITGB1 sequences, we discovered that circITGB1 competitively binds to miR-342-3p and inhibits its expression, which in turn increase the expression of NFAT activating molecule 1 (NFAM1). Based on western blotting and immunological studies, circITGB1 controls dendritic cell maturation by targeting miR-342-3p and NFAM1. circITGB1 also exacerbated cardiac damage and regulated miR-342-3p and NFAM1 expression in a mouse AMI model. This implies that EV-circITGB1 is involved in dendritic cell maturation and cardiac damage via miR-342-3p/NFAM1, and that is linked to AMI-associated pathogenic processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.