DNA methylation in fibrosis

Dowson, Christopher and O'Reilly, Steven (2016) DNA methylation in fibrosis. European Journal of Cell Biology, 95 (9). pp. 323-330. ISSN 0171-9335

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Official URL: https://doi.org/10.1016/j.ejcb.2016.06.003


Fibrosis is characterised by an exuberant wound healing response and the major cell type responsible is the myofibroblast. The myofibroblast is typified by excessive ECM production and contractile activity and is demarcated by alpha-smooth muscle actin expression. What has recently come to light is that the activation of the fibroblast to myofibroblast may be under epigenetic control, specifically methylation. Methylation of DNA is a conserved mechanism to precisely regulate gene expression in a specific context. Hypermethylation leads to gene repression and hypomethylation results in gene induction. Methylation abnormalities have recently been uncovered in fibrosis, both organ specific and widespread fibrosis. The fact that these methylation changes are rapid and reversible lends themselves amenable to therapeutic intervention. This review considers the role of methylation in fibrosis and the activation of the myofibroblasts and how this could be targeted for fibrosis. Fibrosis is of course currently intractable to therapeutics and is a leading cause of morbidity and mortality and is an urgent unmet clinical need.

Item Type: Article
Uncontrolled Keywords: Fibrosis; Systemic sclerosis; Methylation; Methyl cap binding protein; PPAR
Subjects: B900 Others in Subjects allied to Medicine
C400 Genetics
Department: Faculties > Health and Life Sciences > Applied Sciences
Depositing User: Paul Burns
Date Deposited: 05 Jul 2016 11:23
Last Modified: 01 Aug 2021 10:22
URI: http://nrl.northumbria.ac.uk/id/eprint/27228

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