ArticleResearch (Washington, D.C.)2024
A Novel Circular RNA circITGa9 Predominantly Generated in Human Heart Disease Induces Cardiac Remodeling and Fibrosis.
Article in Research (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 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
- Circular RNAs in Cardiovascular Diseases: From Regulatory Networks to Functional Effectors.International journal of molecular sciences · 2026Review
- Circular RNA circFTO promotes pressure overload-induced cardiac hypertrophy by encoding a novel protein FTO-36aa.Journal of thoracic disease · 2025Article
- A new protein isoform encoded by human circular RNA circSLC8a1 contributes to cardiac remodelling.Cardiovascular research · 2025Article
- A Novel Protein NAB1-356 Encoded by circRNA circNAB1 Mitigates Atrial Fibrillation by Reducing Inflammation and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Expanding horizons in theragnostics: from oncology to multidisciplinary applications.La Radiologia medica · 2025Review
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- Recent advances and perspectives on the development of circular RNA cancer vaccines.NPJ vaccines · 2025Review
- Circ-0001283 Aggravates Cardiac Hypertrophy by Targeting Myosin Light Chain 3 Protein.Research (Washington, D.C.) · 2025Article
- Spermine: A prospective treatment for high glucose-induced myocardial fibrosis in db/db mice.Iranian journal of basic medical sciences · 2025Article
- CCN5 Drives Leydig Cell Aging and Testicular Dysfunction: Insights into Fibrosis, Lipid Dysregulation, and Therapeutic Potential.Research (Washington, D.C.) · 2025Article
- A Circular RNA Promotes Tumor Metastasis through Stabilizing MSI2 Protein in Pancreatic Ductal Adenocarcinoma.Research (Washington, D.C.) · 2025Article
- Article
- Review
- A Biomimetic Optical Cardiac Fibrosis-on-a-Chip for High-Throughput Anti-Fibrotic Drug Screening.Research (Washington, D.C.) · 2024Article
- circITGa9: A Novel Therapeutic Target for Cardiac Diseases.Research (Washington, D.C.) · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have highlighted the pivotal roles of circular RNAs (circRNAs) in cardiovascular diseases. Through high-throughput circRNA sequencing of both normal myocardial tissues and hypertrophic patients, we unveiled 32,034 previously undiscovered circRNAs with distinct cardiac expression patterns. Notably, circITGa9, a circRNA derived from integrin-α9, exhibited substantial up-regulation in cardiac hypertrophy patients. This elevation was validated across extensive sample pools from cardiac patients and donors. In vivo experiments revealed heightened cardiac fibrosis in mice subjected to transverse aortic constriction (TAC) after circITGa9 injection. We identified circITGa9 binding proteins through circRNA precipitation followed by liquid chromatography tandem-mass spectrometry. Furthermore, circRNA pull-down/precipitation assays demonstrated that increased circITGa9 expression facilitated binding with tropomyosin 3 (TPM3). Specific binding sites between circITGa9 and TPM3 were identified through computational algorithms and further validated by site-directed mutagenesis. We further showed that circITGa9 induced actin polymerization, characteristic of tissue fibrosis. Finally, we developed approaches that improved cardiac function and decreased fibrosis by delivering small interfering RNA targeting circITGa9 or blocking oligo inhibiting the interaction of circITGa9 and TPM3 into TAC mice, which is amenable for further preclinical and translational development. We conclude that elevated circITGa9 levels drive cardiac remodeling and fibrosis. By pinpointing circITGa9 as a therapeutic target, we open doors to innovative interventions for mitigating cardiac remodeling and fibrosis.
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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.