What can we learn from epigenetics in the year 2009?

被引:30
|
作者
Juengel, Astrid [1 ]
Ospelt, Caroline
Gay, Steffen
机构
[1] Univ Zurich Hosp, Ctr Expt Rheumatol, CH-8091 Zurich, Switzerland
关键词
epigenetics; histone deacetylases; methylation; microRNA; rheumatoid arthritis; sirtuins; sumoylation; HISTONE DEACETYLASE INHIBITORS; RHEUMATOID-ARTHRITIS; GENE-EXPRESSION; DNA HYPOMETHYLATION; MEDIATED ARTHRITIS; SYNOVIAL TISSUE; SIRT1; APOPTOSIS; HYPOXIA; MICE;
D O I
10.1097/BOR.0b013e3283389641
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Rheumatoid arthritis (RA) is a systemic, autoimmune disease resulting in the destruction of affected joints. Even though current therapies with biologics such as tumor necrosis factor-alpha blockers yield significant improvement for the patients, the disease is not curable yet. Therefore, we need novel strategies for better therapies. Recent findings The growing knowledge of epigenetics might give us new insights into the pathogenesis of autoimmune diseases. In the last year, several new findings about epigenetic modifications of gene expression were reported in different arthritides. These modifications describe changes in the expression of DNA that result from methylation, posttranslational modifications of the histone proteins, including acetylation/deacetylation, sumoylation, methylation and microRNAs. Most interestingly, these modifications seem to act in concert and are associated with the circadian metabolic rhythm of cells. Summary This review summarizes reports from the last year about epigenetic modifications of gene expression via acetylation/deacetylation, including sirtuins, sumoylation, methylation, microRNAs in all in rheumatoid arthritis and other arthritides, providing potential strategies for better therapies and encourages the development of specific epigenetic drugs.
引用
收藏
页码:284 / 292
页数:9
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