ArticleAmerican journal of respiratory cell and molecular biology2018
Loss of CDKN2B Promotes Fibrosis via Increased Fibroblast Differentiation Rather Than Proliferation.
Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis.Communications biology · 2026Article
- Peripheral leukocyte transcriptomic changes in preweaned Holstein heifer calves with varying stages of Bovine Respiratory Disease.PloS one · 2026Article
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
- Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine.Frontiers in pharmacology · 2026Review
- CDKN2B Inhibits Vascular Smooth Muscle Phenotypic Switching in Corpus Spongiosum Surrounding the Urethral Plate in Hypospadias.Biomedicines · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- M6Allele: a toolkit for detection of allele-specific RNA N6-methyladenosine modifications.GigaScience · 2025Article
- Genomic regions associated with bovine respiratory disease in pacific northwest Holstein cattle.Frontiers in veterinary science · 2025Article
- The role of epigenetics in pulmonary fibrosis: recent advances in mechanistic insights and therapeutic implications.Frontiers in molecular biosciences · 2025Review
- DNA methylation modification in Idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Article
- The Role of Erythrocyte Membrane Protein Band 4.1-like 3 in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Epigenetics as a versatile regulator of fibrosis.Journal of translational medicine · 2023Review
- More than a Genetic Code: Epigenetics of Lung Fibrosis.Molecular diagnosis & therapy · 2020Review
- Modeling atrial fibrosis in vitro-Generation and characterization of a novel human atrial fibroblast cell line.FEBS open bio · 2020Article
- Impaired Myofibroblast Dedifferentiation Contributes to Nonresolving Fibrosis in Aging.American journal of respiratory cell and molecular biology · 2020Article
- The Role of KCNMB1 and BK Channels in Myofibroblast Differentiation and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease characterized by excessive scarring and fibroblast activation. We previously showed that fibroblasts from patients with IPF are hypermethylated at the CDKN2B gene locus, resulting in decreased CDKN2B expression. Here, we examine how diminished CDKN2B expression in normal and IPF fibroblasts affect fibroblast function, and how loss of CDKN2B contributes to IPF pathogenesis. We first confirmed that protein expression of CDKN2B was diminished in IPF lungs in situ. Loss of CDKN2B was especially notable in regions of increased myofibroblasts and fibroblastic foci. The degree of CDKN2B hypermethylation was particularly elevated in patients with radiographic honeycombing, a marker of more advanced fibrosis, and increased DNA methylation correlated with decreased expression. Although CDKN2B is traditionally considered a cell cycle inhibitor, loss of CDKN2B did not result in an increase in fibroblast proliferation, but instead was associated with an increase in myofibroblast differentiation. An increase in myofibroblast differentiation was not observed when CDKN2A was silenced. Loss of CDKN2B was associated with an increase in the transcription factors serum response factor and myocardin-related transcription factor A, and overexpression of CDKN2B in IPF fibroblasts inhibited myofibroblast differentiation. Finally, decreased CDKN2B expression was noted in fibroblasts from a murine model of fibrosis, and Cdkn2b
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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.