ArticleCell death & disease2020
CircRNA TADA2A relieves idiopathic pulmonary fibrosis by inhibiting proliferation and activation of fibroblasts.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching.International journal of molecular medicine · 2026Article
- Extracellular-Vesicle-Associated Nucleic Acids in the Diagnosis and Treatment of Respiratory Diseases: A Narrative Review.Pharmaceutics · 2026Review
- Circular RNA circSmad4 controls pulmonary fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine.Frontiers in pharmacology · 2026Review
- Deciphering the multifaceted role of circular RNA in aging: from molecular mechanisms to therapeutic potentials.Non-coding RNA research · 2025Review
- CircTADA2A inhibits cell proliferation and promotes ferroptosis by sponging miR-638 in acute myeloid leukemia.Human cell · 2025Article
- Ubiquitin-specific peptidase 10 attenuates bleomycin-induced pulmonary fibrosis via modulating autophagy depending on sirtuin 6-mediated AKT/mTOR.Cell biology and toxicology · 2025Article
- The role of epigenetics in pulmonary fibrosis: recent advances in mechanistic insights and therapeutic implications.Frontiers in molecular biosciences · 2025Review
- Circular RNAs in Organ Fibrosis.Advances in experimental medicine and biology · 2025Review
- Targeting alveolar epithelial cell metabolism in pulmonary fibrosis: Pioneering an emerging therapeutic strategy.Frontiers in cell and developmental biology · 2025Review
- Emerging roles of noncoding RNAs in idiopathic pulmonary fibrosis.Cell death discovery · 2024Review
- Unwinding circular RNA's role in inflammatory pulmonary diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- CircRNA: a rising therapeutic strategy for lung injury induced by pulmonary toxicants.Archives of toxicology · 2024Review
- Head-to-head comparison of relevant cell sources of small extracellular vesicles for cardiac repair: Superiority of embryonic stem cells.Journal of extracellular vesicles · 2024Article
- Article
- Exosomal circRNAs in the plasma serve as novel biomarkers for IPF diagnosis and progression prediction.Journal of translational medicine · 2024Article
- Circular RNAs and their roles in idiopathic pulmonary fibrosis.Respiratory research · 2024Review
- circELP2 reverse-splicing biogenesis and function as a pro-fibrogenic factor by targeting mitochondrial quality control pathway.Journal of cellular and molecular medicine · 2024Article
- circGRHPR inhibits aberrant epithelial-mesenchymal transformation progression of lung epithelial cells associated with idiopathic pulmonary fibrosis.Cell biology and toxicology · 2024Article
- Inhibition of phosphatidylinositol 3-kinase catalytic subunit alpha by miR-203a-3p reduces hypertrophic scar formation via phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway.Burns & trauma · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The excessive activation and proliferation of lung fibroblasts are responsible for the abundant deposition of extracellular matrix (ECM) in idiopathic pulmonary fibrosis (IPF), while its specific mechanism is still unknown. This study focuses on the role of circRNA (circ) TADA2A in functional abnormalities of lung fibroblasts and aims to elaborate its regulatory mechanism. In the present study, circTADA2A was downregulated in both IPF primary human lung fibroblasts and human IPF fibroblastic cell lines. Functionally, the overexpression of circTADA2A repressed the activation and proliferation of normal human fibroblastic cell line induced by several fibrogenic growth factors. Using fluorescence in situ hybridization (FISH), luciferase reporter assays, and RNA pull-down, circTADA2A was confirmed to function as sponges of miR-526b and miR-203, thus releasing the expression of Caveolin (Cav)-1 and Cav2. The overexpression of circTADA2A suppressed lung-fibroblasts activation via Cav1 and reduced lung-fibroblasts proliferation via Cav2. In vivo experiments also confirmed that the overexpression of circTADA2A decreased fibrogenic responses induced by bleomycin in lung-fibrosis mice. Collectively, circTADA2A repressed lung-fibroblasts activation via miR-526b/Cav1 and reduced lung-fibroblasts proliferation via miR-203/Cav2, thus inhibiting the excessive deposition of ECM and relieving IPF.
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