ArticleMolecular medicine reports2021
Long non‑coding RNA HOTTIP enhances the fibrosis of lung tissues by regulating the miR‑744‑5p/PTBP1 signaling axis.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Salvianolic Acid B Upregulates miR-744-5p Expression in Peripheral Blood Mononuclear Cell-Derived Extracellular Vesicles to Alleviate Uremic Cardiomyopathy.Journal of extracellular vesicles · 2026Article
- Biochemical insights and microRNA profiling via next-generation sequencing in moderate and severe COVID-19 cases.Clinics (Sao Paulo, Brazil) · 2026Article
- HOX and MEINOX in cellular plasticity, fibrosis, and cancer.World journal of stem cells · 2025Review
- LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C.Journal of cell communication and signaling · 2024Article
- LncRNA HOTTIP as a diagnostic biomarker for acute respiratory distress syndrome in patients with sepsis and to predict the short-term clinical outcome: a case-control study.BMC anesthesiology · 2024Article
- Polypyrimidine tract binding protein 1 exacerbates cardiac fibrosis by regulating fatty acid-binding protein 5.ESC heart failure · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis of lung tissue can induce the occurrence and development of numerous types of lung disease. The expression levels of the long non‑coding RNA (lncRNA) HOXA distal transcript antisense RNA (HOTTIP) have been reported to be upregulated during the development of fibrosis in liver tissues, which subsequently activated hepatic stellate cells. However, whether the lncRNA HOTTIP participates in the occurrence and development of lung fibrosis remains unknown. The present study aimed to investigate the role of lncRNA HOTTIP in lung fibrosis and its potential mechanism. In the present study, A549 cells were stimulated with TGF‑β1 to induce lung fibrosis
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