ArticleAmerican journal of respiratory and critical care medicine2013
Epigenetic regulation of miR-17~92 contributes to the pathogenesis of pulmonary fibrosis.
Article in American journal of respiratory and critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 2 of them syntheses that pooled it.
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Who cites it
148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 265 citations in OpenAlex.
- Systematic review of overlapping microRNA patterns in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2023Pooled it
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Exploring the role of epigenetics in the processes related to the development of endometrosis in the mare.The Journal of reproduction and development · 2026Review
- miR-17-5p: bridging the gap between disease mechanisms and therapeutic innovations.Epigenomics · 2025Review
- Methylome-driven regulation of miRNA expression and its relationship to cardiac dysfunction in idiopathic dilated cardiomyopathy.Clinical epigenetics · 2025Article
- Construction and Bioinformatics Analysis of ceRNA Regulatory Networks in Idiopathic Pulmonary Fibrosis.Biochemical genetics · 2025Article
- LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation.Cellular and molecular life sciences : CMLS · 2025Article
- Key Amniotic Fluid miRNAs as Promising Target Molecules for the Antenatal Prevention of Pulmonary Hypoplasia Associated with Congenital Diaphragmatic Hernia.International journal of molecular sciences · 2025Article
- MiR-29a-3p inhibits fibrosis of diabetic kidney disease in diabetic miceWorld journal of diabetes · 2025Article
- Review
- An Overview of the Role of Genetic factors in Idiopathic Pulmonary Fibrosis: Insights from Epidemiology to Prognosis.International journal of medical sciences · 2025Review
- Mir-155-5p targets TP53INP1 to promote proliferative phenotype in hypersensitivity pneumonitis lung fibroblasts.Non-coding RNA research · 2024Article
- Genetics and Genomics of Pulmonary Fibrosis: Charting the Molecular Landscape and Shaping Precision Medicine.American journal of respiratory and critical care medicine · 2024Review
- Methylation of microRNA genes and its effect on secondary xylem development of stem in poplar.The plant genome · 2024Article
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- DNA methylation modification in Idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Pulmonary Fibrosis and Diabetes Mellitus: Two coins with the same face.Archives of internal medicine research · 2024Article
- The Plastic Interplay between Lung Regeneration Phenomena and Fibrotic Evolution: Current Challenges and Novel Therapeutic Perspectives.International journal of molecular sciences · 2023Review
- Prognostic significance of serum miR-18a-5p in severe COVID-19 Egyptian patients.Journal, genetic engineering & biotechnology · 2023Article
88 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
rationaleIdiopathic pulmonary fibrosis (IPF) is a disease of progressive lung fibrosis with a high mortality rate. In organ repair and remodeling, epigenetic events are important. MicroRNAs (miRNAs) regulate gene expression post-transcriptionally and can target epigenetic molecules important in DNA methylation. The miR-17~92 miRNA cluster is critical for lung development and lung epithelial cell homeostasis and is predicted to target fibrotic genes and DNA methyltransferase (DNMT)-1 expression.
objectivesWe investigated the miR-17~92 cluster expression and its role in regulating DNA methylation events in IPF lung tissue.
methodsExpression and DNA methylation patterns of miR-17~92 were determined in human IPF lung tissue and fibroblasts and fibrotic mouse lung tissue. The relationship between the miR-17~92 cluster and DNMT-1 expression was examined in vitro. Using a murine model of pulmonary fibrosis, we examined the therapeutic potential of the demethylating agent, 5'-aza-2'-deoxycytidine. MEASUREMENTS AND MAIN
resultsCompared with control samples, miR-17~92 expression was reduced in lung biopsies and lung fibroblasts from patients with IPF, whereas DNMT-1 expression and methylation of the miR-17~92 promoter was increased. Several miRNAs from the miR-17~92 cluster targeted DNMT-1 expression resulting in a negative feedback loop. Similarly, miR-17~92 expression was reduced in the lungs of bleomycin-treated mice. Treatment with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pulmonary fibrosis model reduced fibrotic gene and DNMT-1 expression, enhanced miR-17~92 cluster expression, and attenuated pulmonary fibrosis.
conclusionsThis study provides insight into the pathobiology of IPF and identifies a novel epigenetic feedback loop between miR-17~92 and DNMT-1 in lung fibrosis.
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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.