ArticleCell death & disease2022
The histone methyltransferase DOT1L is a new epigenetic regulator of pulmonary fibrosis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- DOT1L Drives Endothelial-to-Mesenchymal Transition and Fibrotic Vascular Remodeling via H3K79 Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- The role of histone methylation in fibrosis and its therapeutic potential.Journal of translational medicine · 2026Review
- SPARC Drives Tubulointerstitial Fibrosis through Regulating the CBP-DOT1L Pathway.International journal of biological sciences · 2026Article
- Molecular mechanisms of lung injury from ultra high and conventional dose rate pulsed radiation based on 4D DIA proteomics study.Scientific reports · 2025Article
- The histone demethylase KDM6B links obstructive sleep apnea to idiopathic pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Progressive lung fibrosis: reprogramming a genetically vulnerable bronchoalveolar epithelium.The Journal of clinical investigation · 2025Review
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- Dot1l Regulates the Spontaneous Bone Regeneration of Periosteum-Derived Stem Cells by Regulating Chac1 Expression.Stem cells international · 2025Article
- The role of epigenetics in pulmonary fibrosis: recent advances in mechanistic insights and therapeutic implications.Frontiers in molecular biosciences · 2025Review
- Epigenetic modification in liver fibrosis: Promising therapeutic direction with significant challenges ahead.Acta pharmaceutica Sinica. B · 2024Review
- Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024Review
- The disruptor of telomeric silencing 1-like (DOT1L) promotes peritoneal fibrosis through the upregulation and activation of protein tyrosine kinases.Molecular biomedicine · 2024Article
- Mechanisms underlying the involvement of peritoneal macrophages in the pathogenesis and novel therapeutic strategies for dialysis-induced peritoneal fibrosis.Frontiers in immunology · 2024Review
- Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly.Respiratory research · 2023Article
- The evaluation of six genes combined value in glioma diagnosis and prognosis.Journal of cancer research and clinical oncology · 2023Article
- A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023Review
- High-Fat Diet Related Lung Fibrosis-Epigenetic Regulation Matters.Biomolecules · 2023Review
- Identification of immune biomarkers associated with basement membranes in idiopathic pulmonary fibrosis and their pan-cancer analysis.Frontiers in genetics · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with increasing occurrence, high death rates, and unfavorable treatment regimens. The pathogenesis underlying IPF is complex and the epigenetic contributions to IPF are largely unknown. Recent studies have shown that DOT1L (Disruptor of telomeric silencing-1 like), a histone H3K79 methyltransferase, contributes to fibrosis response, but its role in IPF remains unclear. DOT1L, H3K79me3, and the profibrotic proteins levels were upregulated in the pulmonary fibrosis models both in vivo and in vitro. Lentivirus-mediated DOT1L knockdown or DOT1L-specific inhibitor EPZ5676 alleviated the pathogenesis of bleomycin-induced mouse pulmonary fibrosis. Furthermore, heterozygous DOT1L-deficient mice (Dot1l
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.