ArticleCell death & disease2022
Systematic analyses identify the anti-fibrotic role of lncRNA TP53TG1 in IPF.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- A Lung-Targeted Carrier of Carbon Monoxide for Idiopathic Pulmonary Fibrosis Therapy.ACS nano · 2026Article
- The Relationship Between Differential Expression of Non-coding RNAs (TP53TG1, LINC00342, MALAT1, DNM3OS, miR-126-3p, miR-200a-3p, miR-18a-5p) and Protein-Coding Genes (PTEN, FOXO3) and Risk of Idiopathic Pulmonary Fibrosis.Biochemical genetics · 2026Article
- Mechanosensitive genomic enhancers potentiate the cellular response to matrix stiffness.Science (New York, N.Y.) · 2025Article
- The regulating markers for Brucella spondylitis and tuberculous spondylitis.BMC infectious diseases · 2025Article
- LncRNA TP53TG1 promotes the growth and osteo/dentinogenic differentiation of dental pulp stem cells by activating the Smad3 and JNK1/2 pathway.In vitro cellular & developmental biology. Animal · 2025Article
- A multimorphic variant in ThPOK causes an inborn error of immunity with T cell defects and fibrosis.The Journal of experimental medicine · 2025Article
- Convergent evolution in high-altitude and marine mammals: Molecular adaptations to pulmonary fibrosis and hypoxia.Zoological research · 2024Article
- Article
- Integrative bioinformatics and validation studies reveal KDM6B and its associated molecules as crucial modulators in Idiopathic Pulmonary Fibrosis.Frontiers in immunology · 2023Article
- Non-Coding RNAs in Regulating Plaque Progression and Remodeling of Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2022Review
- Knockdown of lncRNA TP53TG1 Enhances the Efficacy of Sorafenib in Human Hepatocellular Carcinoma Cells.Non-coding RNA · 2022Article
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Authors and funding
21 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) was reported to be a critical regulator of cellular homeostasis, but poorly understood in idiopathic pulmonary fibrosis (IPF). Here, we systematically identified a crucial lncRNA, p53-induced long non-coding RNA TP53 target 1 (TP53TG1), which was the dysregulated hub gene in IPF regulatory network and one of the top degree genes and down-regulated in IPF-drived fibroblasts. Functional experiments revealed that overexpression of TP53TG1 attenuated the increased expression of fibronectin 1 (Fn1), Collagen 1α1, Collagen 3α1, ACTA2 mRNA, Fn1, and Collagen I protein level, excessive fibroblasts proliferation, migration and differentiation induced by TGF-β1 in MRC-5 as well as PMLFs. In vivo assays identified that forced expression of TP53TG1 by adeno-associated virus 5 (AAV5) not only prevented BLM-induced experimental fibrosis but also reversed established lung fibrosis in the murine model. Mechanistically, TP53TG1 was found to bind to amount of tight junction proteins. Importantly, we found that TP53TG1 binds to the Myosin Heavy Chain 9 (MYH9) to inhibit its protein expression and thus the MYH9-mediated activation of fibroblasts. Collectively, we identified the TP53TG1 as a master suppressor of fibroblast activation and IPF, which could be a potential hub for targeting treatment of the disease.
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