ArticleAging2021
circACTA2 mediates Ang II-induced VSMC senescence by modulation of the interaction of ILF3 with CDK4 mRNA.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Decoding noncoding RNAs in regulating cardiovascular aging and age-related conditions: the emerging landscape.Science China. Life sciences · 2026Review
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- Functions and application of circRNAs in vascular aging and aging-related vascular diseases.Journal of nanobiotechnology · 2025Review
- Macrophage ILF3 promotes abdominal aortic aneurysm by inducing inflammatory imbalance in male mice.Nature communications · 2024Article
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- Non-Coding Ribonucleic Acids as Diagnostic and Therapeutic Targets in Cardiac Fibrosis.Current heart failure reports · 2024Review
- Comparative Analysis of Circular RNAs Expression and Function between Aortic and Intracranial Aneurysms.Current drug targets · 2024Review
- Targeting Vascular Smooth Muscle Cell Senescence: A Novel Strategy for Vascular Diseases.Journal of cardiovascular translational research · 2023Review
- circACTA2 inhibits NLRP3 inflammasome-mediated inflammation via interacting with NF-κB in vascular smooth muscle cells.Cellular and molecular life sciences : CMLS · 2023Article
- Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?Journal of clinical medicine · 2023Review
- Down-regulation of the Smad signaling by circZBTB46 via the Smad2-PDLIM5 axis to inhibit type I collagen expression.Journal of geriatric cardiology : JGC · 2023Article
- Circular RNAs as a Diagnostic and Therapeutic Target in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- SF3B4 promotes Twist1 expression and clear cell renal cell carcinoma progression by facilitating the export of KLF 16 mRNA from the nucleus to the cytoplasm.Cell death & disease · 2023Article
- The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022Review
- Resveratrol alleviates Ang II-induced vascular smooth muscle cell senescence by upregulating E2F1/SOD2 axis.Toxicology research · 2022Article
- ERα/β/DMP1 axis promotes trans-differentiation of chondrocytes to bone cells through GSK-3β/β-catenin pathway.Journal of anatomy · 2022Article
- Circular RNAs: regulators of vascular smooth muscle cells in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- E2F6/KDM5C promotes SF3A3 expression and bladder cancer progression through a specific hypomethylated DNA promoter.Cancer cell international · 2022Article
- Cellular Senescence in Cardiovascular Diseases: A Systematic Review.Aging and disease · 2022Review
- Emerging Role of Non-Coding RNAs in Senescence.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic angiotensin II (Ang II) stimulation induces vascular smooth muscle cell (VSMC) senescence, and circRNAs and members of the ILF3 family are implicated in cellular senescence, but the mechanism underlying regulation of circRNAs and ILF3 by Ang II in VSMCs remains poorly understood. Here, a model of Ang II-induced VSMC senescence and the renal artery of hypertensive patients were used to investigate the roles and mechanisms of circACTA2 and ILF3 in VSMC senescence. We show that circACTA2 expression was elevated in Ang II-stimulated VSMCs and in the vascular walls of hypertensive patients. circACTA2 knockdown largely abrogated Ang II-induced VSMC senescence as shown by decreased p21 expression and increased CDK4 expression as well as by decreased SA β-gal-positive cells. Oligo pull-down and RIP assays revealed that both circACTA2 and CDK4 mRNA could bind with ILF3, and Ang II facilitated circACTA2 association with ILF3 and attenuated ILF3 interaction with CDK4 mRNA. Mechanistically, increased circACTA2 by Ang II reduced ILF3 association with CDK4 mRNA by competing with CDK4 mRNA to bind to ILF3, which decreases CDK4 mRNA stability and protein expression, thus leading to Ang II-induced VSMC senescence. Targeting the circACTA2-ILF3-CDK4 axis may provide a novel therapeutic strategy for VSMC senescence-associated cardiovascular diseases.
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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.