ArticleScience China. Life sciences2024
Fibroblast-localized lncRNA CFIRL promotes cardiac fibrosis and dysfunction in dilated cardiomyopathy.
Article in Science China. Life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Endothelial S1PR3 downregulation exacerbates pressure overload-induced cardiac remodeling by promoting fibrosis and inflammation.Science China. Life sciences · 2026Article
- Ellagic acid attenuates myocardial fibrosis by suppressing Bmi1-mediated inhibition of the p53/p21 pathway in cardiac fibroblasts.Molecular and cellular biochemistry · 2026Article
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Dual recombinase-mediated genetic labeling and selective ablation of fibroblasts.Science China. Life sciences · 2026Article
- The Impact of Maternal Obesity and Diabetes on the Development of Congenital Heart Defects (CHDs) in Offspring: A Narrative Review.Metabolites · 2026Review
- LncRNA CARD8-AS1 acts as a potential novel biomarker and promotes atrial fibrillation progression via the miR-31-5p/ARRB1 pathway.Molecular genetics and genomics : MGG · 2026Article
- Bovine milk exosomes influence transcriptome profiles and reduce cardiac fibrosis in a rat model.Scientific reports · 2025Article
- Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025Review
- Isorhamnetin Attenuates Isoproterenol-Induced Myocardial Injury by Reducing ENO1 (Alpha-Enolase) in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2025Article
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
- Cardiomyopathies: The Role of Non-Coding RNAs.Non-coding RNA · 2024Review
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Authors and funding
12 authors.
Funding
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Abstract
CFIRL is a long noncoding RNA (lncRNA), we previously identified as the most significantly upregulated lncRNA in the failing hearts of patients with dilated cardiomyopathy (DCM). In this study, we determined the function of CFIRL and its role in DCM. Real-time polymerase chain reaction and in situ hybridization assays revealed that CFIRL was primarily localized in the nucleus of cardiac fibroblasts and robustly increased in failing hearts. Global knockdown or fibroblast-specific knockout of CFIRL attenuated transverse aortic constriction (TAC)-induced cardiac dysfunction and fibrosis in vivo. Overexpression of CFIRL in vitro promoted fibroblast proliferation and aggravated angiotensin II-induced differentiation to myofibroblasts. CFIRL knockdown attenuated these effects. Mechanistically, RNA pull-down assay and gene expression profiling revealed that CFIRL recruited ENO1, a newly identified noncanonical transcriptional factor, to activate IL-6 transcription. IL-6 exerted a paracrine effect on cardiomyocytes to promote cardiac hypertrophy, which can be prevented by CFIRL knockdown. These findings uncover the critical role of CFIRL, a fibroblast-associated lncRNA, in heart failure by facilitating crosstalk between fibroblasts and cardiomyocytes. CFIRL knockdown might be a potent strategy to prevent cardiac remodeling in heart failure, particularly in DCM.
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