Journal
RHEUMATOLOGY
Volume 54, Issue 10, Pages 1759-1770Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keu155
Keywords
epigenetic; scleroderma; DNA methylation; histone modifications; endothelial cells; fibroblasts; fibrosis; nitric oxide synthase; friend leukaemia integration 1 transcription factor; microRNA
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Funding
- University of Toledo, School of Medicine
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The objective of this review is to present evidence that supports the central role of epigenetic regulation in the pathogenesis of SSc. SSc is a complex autoimmune disease characterized by immune activation, fibrosis of the skin and internal organs and obliterative vasculopathy affecting predominantly the microvessels. Remarkable progress has been made in the past few years emphasizing the importance of epigenetic modifications in the pathogenesis of many disorders, including SSc. Current evidence demonstrates alterations in DNA methylation, histone code modifications and changes in microRNA (miRNA) expression levels in SSc cells. Recent reports have described the differential expression of numerous regulatory miRNAs in SSc, mainly in SSc fibroblasts, a number of which are important in TGF-beta pathways and downstream signalling cascades. While studies to date have revealed the significant role of epigenetic modifications in the pathogenesis of SSc, the causal nature of epigenetic alterations in SSc pathogenesis remains elusive. Additional longitudinal and comprehensive epigenetic studies designed to evaluate the effect of environmental epigenetic factors on disease pathogenesis are needed.
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