Epigenetics in the treatment of systemic lupus erythematosus: Potential clinical application

被引：31

作者：

Guo, Yu ^{[1
,2
]}

Sawalha, Amr H. ^{[3
]}

Lu, Qianjin ^{[1
,2
]}

机构：

[1] Cent S Univ, Xiangya Hosp 2, Dept Dermatol, Changsha 410011, Hunan, Peoples R China

[2] Cent S Univ, Xiangya Hosp 2, Epigenet Res Ctr, Changsha 410011, Hunan, Peoples R China

[3] Univ Michigan, Dept Internal Med, Div Rheumatol, Ann Arbor, MI 48109 USA

来源：

CLINICAL IMMUNOLOGY | 2014年 / 155卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Systemic lupus erythematosus (SLE); Biomarkers; Pharmacoepigenetics; HDAC inhibitors; DNA methylation; microRNA; CD4(+) T-CELLS; DEACETYLASE INHIBITOR ITF2357; ABNORMAL DNA METHYLATION; TRANS-RETINOIC ACID; IN-VIVO; DISEASE-ACTIVITY; RHEUMATOID-ARTHRITIS; TOTAL GLUCOSIDES; SIGNALING PROTEINS; IMMUNE-RESPONSES;

D O I：

10.1016/j.clim.2014.09.002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The current treatments of systemic lupus erythematosus (SLE) have been based on the use of immunosuppressive drugs which are linked to serious side effects. The more effective therapeutic approaches with minimal or no side effects for SLE patients are hard to develop, mainly due to the complexity of the disease. The discovery of pharmacoepigenetics provides a new way to solve this problem. Epigenetic modifications can influence drug efficacy by altering gene expression via changing chromatin structure. Although still in early development, epigenetic studies in SLE are expected to reveal novel therapeutic targets and disease biomarkers in autoimmunity. For example, miRNAs, which have been identified to govern many genes including drug targets, are altered in disease development and after drug administration. This review aims to present an overview of current epigenetic mechanisms involved in the pathogenesis of SLE, and discuss their potential roles in clinical and pharmacological applications. (C) 2014 Elsevier Inc. All rights reserved.

引用

页码：79 / 90

页数：12

共 119 条

[1]

Protein Phosphatase 2A Enables Expression of Interleukin 17 (IL-17) through Chromatin Remodeling [J].