ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019
lncITPF Promotes Pulmonary Fibrosis by Targeting hnRNP-L Depending on Its Host Gene ITGBL1.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Epigenetic regulatory mechanisms and translational applications in idiopathic pulmonary fibrosis.American journal of clinical and experimental immunology · 2026Review
- HBV activates hepatic stellate cells through RUNX2/ITGBL1 axis.Virology journal · 2025Article
- YTHDC1 phase separation drives the nuclear export of mCell death & disease · 2025Article
- Integrated analysis of bioinformatics, mendelian randomization, and experimental validation reveals novel diagnostic and therapeutic targets for osteoarthritis: progesterone as a potential therapeutic agent.Journal of orthopaedic surgery and research · 2025Article
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Pathogenic mycoplasmas of humans regulate the long noncoding RNAs in epithelial cells.Non-coding RNA research · 2023Article
- Article
- LncRNAActa pharmaceutica Sinica. B · 2022Article
- MOBT Alleviates Pulmonary Fibrosis through an lncITPF-hnRNP-l-Complex-Mediated Signaling Pathway.Molecules (Basel, Switzerland) · 2022Article
- Long Non-Coding RNAs in Cardiac and Pulmonary Fibroblasts and Fibrosis.Non-coding RNA · 2022Article
- Small extracellular vesicles derived from dermal fibroblasts promote fibroblast activity and skin development through carrying miR-218 and ITGBL1.Journal of nanobiotechnology · 2022Article
- hnRNPL-activated circANKRD42 back-splicing and circANKRD42-mediated crosstalk of mechanical stiffness and biochemical signal in lung fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Danshensu methyl ester enhances autophagy to attenuate pulmonary fibrosis by targeting lncIAPF-HuR complex.Frontiers in pharmacology · 2022Article
- Epigenetics alternation in lung fibrosis and lung cancer.Frontiers in cell and developmental biology · 2022Review
- A Novel Regulatory Player in the Innate Immune System: Long Non-Coding RNAs.International journal of molecular sciences · 2021Review
- Long Noncoding RNAInternational journal of molecular sciences · 2021Article
- Construction of a Myc-associated ceRNA network reveals a prognostic signature in hepatocellular carcinoma.Molecular therapy. Nucleic acids · 2021Article
- Long non-coding RNA MFAT1 promotes skeletal muscle fibrosis by modulating the miR-135a-5p-Tgfbr2/Smad4 axis as a ceRNA.Journal of cellular and molecular medicine · 2021Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of long non-coding RNA (lncRNA) in idiopathic pulmonary fibrosis (IPF) is poorly understood. We found a novel lncRNA-ITPF that was upregulated in IPF. Bioinformatics and in vitro translation verified that lncITPF is an actual lncRNA, and its conservation is in evolution. Northern blot and rapid amplification of complementary DNA ends were used to analyze the full-length sequence of lncITPF. RNA fluorescence in situ hybridization and nucleocytoplasmic separation demonstrated that lncITPF was mainly located in the nucleus. RNA sequencing, chromatin immunoprecipitation (ChIP)-qPCR, CRISPR-Cas9 technology, and promoter activity analysis showed that the fibrotic function of lncITPF depends on its host gene integrin β-like 1 (ITGBL1), but they did not share the same promoter and were not co-transcribed. Luciferase activity, pathway inhibitors, and ChIP-qPCR showed that smad2/3 binds to the lncITPF promoter, and TGF-β1-smad2/3 was the upstream inducer of the fibrotic pathway. Furthermore, RNA-protein pull-down, liquid chromatography-mass spectrometry (LC-MS), and protein-RNA immunoprecipitation showed that lncITPF regulated H3 and H4 histone acetylation in the ITGBL1 promoter by targeting heterogeneous nuclear ribonucleoprotein L. Finally, sh-lncITPF was used to evaluate the therapeutic effect of lncITPF. Clinical analysis showed that lncITPF is associated with the clinicopathological features of IPF patients. Our findings provide a therapeutic target or diagnostic biomarker for IPF.
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Registered trials
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