Epigenetics in SLE
- PMID: 28752494
- PMCID: PMC5532407
- DOI: 10.1007/s11926-017-0685-1
Epigenetics in SLE
Abstract
Purpose of review: Systemic lupus erythematosus is a severe autoimmune/inflammatory condition of unknown pathophysiology. Though genetic predisposition is essential for disease expression, risk alleles in single genes are usually insufficient to confer disease. Epigenetic dysregulation has been suggested as the missing link between genetic risk and the development of clinically evident disease.
Recent findings: Over the past decade, epigenetic events moved into the focus of research targeting the molecular pathophysiology of SLE. Epigenetic alteration can be the net result of preceding infections, medication, diet, and/or other environmental influences. While altered DNA methylation and histone modifications had already been established as pathomechanisms, DNA hydroxymethylation was more recently identified as an activating epigenetic mark. Defective epigenetic control contributes to uncontrolled cytokine and co-receptor expression, resulting in immune activation and tissue damage in SLE. Epigenetic alterations promise potential as disease biomarkers and/or future therapeutic targets in SLE and other autoimmune/inflammatory conditions.
Keywords: Epigenetic; Histone; Hydroxymethylation; Inflammation; Lupus; Methylation; Non-coding RNA.
Conflict of interest statement
Conflict of Interest
Christian Hedrich declares grants from Fritz-Thyssen Foundation Research and MeDDrive and grants pending from Novartis Pharmaceuticals.
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by any of the authors.
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