DNA Methylome Alterations Are Associated with Airway Macrophage Differentiation and Phenotype during Lung Fibrosis

McErlean, Peter; Bell, Christopher G.; Hewitt, Richard; Busharat, Zabreen; Ogger, Patricia P.; Ghai, Poonam; Albers, G J; Calamita, Emily; Kingston, Shaun; Molyneaux, Philip L.; Beck, Stephan; Lloyd, Clare M.; Maher, Toby M.; Byrne, Adam

doi:10.1164/rccm.202101-0004oc

Cited by 19 publications

(24 citation statements)

References 84 publications

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“…M2 macrophages are actively involved in the pathogenesis of pulmonary fibrosis (Wang et al, 2020). Furthermore, there is compelling evidence that DNA methylation, one of the main epigenetic mechanisms, is also involved in the pathogenesis of pulmonary fibrosis (Sanders et al, 2012;McErlean et al, 2021). In this regard, there are proteins called MBD, in particular MBD2, which by binding to these methylated areas mediate their activation or repression.…”

Section: Role Of Macrophagesmentioning

confidence: 99%

“…Going into more detail, MBD2 improves PI3K/Akt signaling to promote the M2 program of macrophages and consequently the fibrogenesis process. All this is extremely important because MBD2 was found to be highly expressed in pulmonary macrophages of patients with COVID19 and that the loss of MBD2 leads to a marked reduction in the accumulation of M2 macrophages in the lung, with a reduction in fibrotic commitment (Wang et al, 2021b;McErlean et al, 2021).…”

Section: Role Of Macrophagesmentioning

confidence: 99%

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Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

et al. 2022

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The pathogenetic mechanism of post-Covid-19 pulmonary fibrosis is currently a topic of intense research interest, but still largely unexplored. The aim of this work was to carry out a systematic exploratory search of the literature (Scoping review) to identify and systematize the main pathogenetic mechanisms that are believed to be involved in this phenomenon, in order to highlight the same molecular aspect of the lung. These aims could be essential in the future for therapeutic management. We identified all primary studies involving in post COVID19 syndrome with pulmonary fibrosis as a primary endpoint by performing data searches in various systematic review databases. Two reviewers independently reviewed all abstracts (398) and full text data. The quality of study has been assess through SANRA protocol. A total of 32 studies involving were included, included the possible involvement of inflammatory cytokines, concerned the renin-angiotensin system, the potential role of galectin-3, epithelial injuries in fibrosis, alveolar type 2 involvement, Neutrophil extracellular traps (NETs) and the others implied other specific aspects (relationship with clinical and mechanical factors, epithelial transition mesenchymal, TGF-β signaling pathway, midkine, caspase and macrophages, genetics). In most cases, these were narrative reviews or letters to the editor, except for 10 articles, which presented original data, albeit sometimes in experimental models. From the development of these researches, progress in the knowledge of the phenomenon and hopefully in its prevention and therapy may originate.

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Section: Role Of Macrophagesmentioning

confidence: 99%

Section: Role Of Macrophagesmentioning

confidence: 99%

Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

et al. 2022

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“…Targeting epigenome represents a potential strategy for fibrosis treatment. Changes in the epigenome are associated with the development and function of AMsin the IPF lung (136,137). Most methylation changes have been identified outside of CpG islands and several gene expression signatures have been reported known (e.g., collagens, HDAC4, NOTCH1, PDGF, SERPINF1, and TOLLIP) and novel candidate (CASZ1) genes.…”

Section: Epigeneticsmentioning

confidence: 99%

The oncogenic landscape of the idiopathic pulmonary fibrosis: a narrative review

Stella¹,

D’Agnano²,

Piloni³

et al. 2022

Transl Lung Cancer Res

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Background and Objective: Translational research is a source of continuous innovation in medicine, more particularly for clinical research on new treatment modalities in idiopathic pulmonary fibrosis (IPF) patients.However, the heterogeneity of the disease is well recognized, and different pathological and molecular settings have been identified. The molecular mechanisms by which IPF proceeds in time and space remains poorly understood. Although some IPF features are reminiscent of cancer, the dynamics of malignant divergent clonal selective pressure and heterogeneity clearly differ from those occurring in IPF. This is reflected in the absence of patient proper selection and stratification to biological agents (pirfenidone, nintedanib) which limit therapeutic efficacy. Consequently, increased costs are related to the clinical management of advanced IPF patients. Steady collaboration and fluid communication between pneumo-oncologists, radiologists and molecular biologists is a clear priority for the correct interpretation of tests and the definition of effective personalized strategies against this orphan disease. The present work aims at providing the most relevant hints shared by cancer and IPF.Methods: A systematic literature review was performed to identify all relevant data. The examined databases were Scopus, Web of Science, Cochrane, Google Scholar, and PubMed. The last search was run on January 5, 2022. We have primarily conducted separated research for lung cancer, IPF, genetics, epigenetics, surgery in IPF and cancer.

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“…In this issue of the Journal , McErlean and colleagues (pp. 954–966 ) investigate the role of DNA methylation in altering airway macrophage gene expression during pulmonary fibrosis ( 8 ). The authors examine the DNA methylation profile of alveolar macrophages isolated from patients with IPF and control subjects and compared these data with established Blueprint datasets from representative myeloid cells, including monocyte subtypes and in vitro –derived macrophages ( 8 ).…”

mentioning

confidence: 99%

“…954–966 ) investigate the role of DNA methylation in altering airway macrophage gene expression during pulmonary fibrosis ( 8 ). The authors examine the DNA methylation profile of alveolar macrophages isolated from patients with IPF and control subjects and compared these data with established Blueprint datasets from representative myeloid cells, including monocyte subtypes and in vitro –derived macrophages ( 8 ). They determine that the majority of the myeloid-specific CpGs (regions of DNA containing cytosine-guanine nucleotides connected by phosphodiester bond) reside in intronic or intergeneic regions and correlate with open chromatin motifs (as determined by DNase-1 hypersensitivity sites).…”

mentioning

confidence: 99%

The Epigenomic Landscape: A Cornerstone of Macrophage Phenotype Regulation in the Fibrotic Lung

Ballinger

Mora

2021

Am J Respir Crit Care Med

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DNA Methylome Alterations Are Associated with Airway Macrophage Differentiation and Phenotype during Lung Fibrosis

Cited by 19 publications

References 84 publications

Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

The oncogenic landscape of the idiopathic pulmonary fibrosis: a narrative review

The Epigenomic Landscape: A Cornerstone of Macrophage Phenotype Regulation in the Fibrotic Lung

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