ArticleScience China. Life sciences2023
LncRNA CFAR promotes cardiac fibrosis via the miR-449a-5p/LOXL3/mTOR axis.
Article in Science China. Life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Lysyl oxidase (LOX) family proteins in extracellular matrix homeostasis: roles in disease and radiation-induced pathogenesis.Molecular biology reports · 2026Review
- The "dual personality" of LOXL3: a tumor accomplice and a new hope for immunotherapy.Human cell · 2025Review
- Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Unveiling the clinical significance of RNA pseudouridine in colorectal cancer.Science China. Life sciences · 2025Article
- Integrated Proteomics and Metabolomics Analyses Reveal Molecular Mechanism of Cardiac Resynchronization Therapy Against Cardiac Fibrosis and Ventricular Arrhythmias.Cardiovascular toxicology · 2025Article
- LncRNA-5829: a novel inhibitor of cardiac fibrosis.Cardiovascular diagnosis and therapy · 2025Article
- A secretome atlas of cardiac fibroblasts from healthy and infarcted mouse hearts.Communications biology · 2025Article
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- Mesenchymal stem cells derived exosomes: a new era in cardiac regeneration.Stem cell research & therapy · 2025Review
- Inhibition of high glucose-induced cardiac fibroblast activation: an effective treatment for diabetic cardiomyopathy using Chinese herbal medicine.Frontiers in pharmacology · 2025Review
- Hydrogen sulfide alleviates high-salt-stimulated myocardial fibrosis through inhibiting hypoxia-inducible factor-1α.Frontiers in pharmacology · 2025Article
- miR-449a: A Promising Biomarker and Therapeutic Target in Cancer and Other Diseases.Cell biochemistry and biophysics · 2024Review
- Fibroblast-localized lncRNA CFIRL promotes cardiac fibrosis and dysfunction in dilated cardiomyopathy.Science China. Life sciences · 2024Article
- Regulation of insect behavior by non-coding RNAs.Science China. Life sciences · 2024Review
- Pivotal role for long noncoding RNAs in zygotic genome activation in mice.Science China. Life sciences · 2024Article
- Targeting lncRNA16 by GalNAc-siRNA conjugates facilitates chemotherapeutic sensibilization via the HBB/NDUFAF5/ROS pathway.Science China. Life sciences · 2024Article
- Regulatory mechanisms of long non-coding RNAs on mitochondrial function in congestive heart failure.Non-coding RNA research · 2024Review
- Melatonin decreases GSDME mediated mesothelial cell pyroptosis and prevents peritoneal fibrosis and ultrafiltration failure.Science China. Life sciences · 2024Article
- Non-coding RNAs: targets for Chinese herbal medicine in treating myocardial fibrosis.Frontiers in pharmacology · 2024Review
- Multifaced roles of desmoplastic reaction and fibrosis in pancreatic cancer progression: Current understanding and future directions.Cancer science · 2023Review
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis is one of the crucial pathological factors in the heart, and various cardiac conditions associated with excessive fibrosis can eventually lead to heart failure. However, the exact molecular mechanism of cardiac fibrosis remains unclear. In the present study, we show that a novel lncRNA that we named cardiac fibrosis-associated regulator (CFAR) is a profibrotic factor in the heart. CFAR was upregulated in cardiac fibrosis and its knockdown attenuated the expression of fibrotic marker genes and the proliferation of cardiac fibroblasts, thereby ameliorating cardiac fibrosis. Moreover, CFAR acted as a ceRNA sponge for miR-449a-5p and derepressed the expression of LOXL3, which we experimentally established as a target gene of miR-449a-5p. In contrast to CFAR, miR-449a-5p was found to be significantly downregulated in cardiac fibrosis, and artificial knockdown of miR-449a-5p exacerbated fibrogenesis, whereas overexpression of miR-449a-5p impeded fibrogenesis. Furthermore, we found that LOXL3 mimicked the fibrotic factor TGF-β1 to promote cardiac fibrosis by activating mTOR. Collectively, our study established CFAR as a new profibrotic factor acting through a novel miR-449a-5p/LOXL3/mTOR axis in the heart and therefore might be considered as a potential molecular target for the treatment of cardiac fibrosis and associated heart diseases.
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