The real culprit in systemic lupus erythematosus: abnormal epigenetic regulation.
The real culprit in systemic lupus erythematosus: abnormal epigenetic regulation.
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DOI：
10.3390/ijms160511013
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发表时间：
2015-05-15
影响因子：
5.6
通讯作者：
Lu Q
中科院分区：
文献类型：
--
作者：
Wu H;Zhao M;Chang C;Lu Q
系统性红斑狼疮（SLE）是一种自身免疫性疾病，涉及多个器官和抗核抗体的存在。SLE的发病机制已被深入研究，但仍远不清楚。B和T淋巴细胞异常、细胞凋亡失调、细胞凋亡物质清除缺陷以及各种遗传和表观遗传因素可导致SLE的发生。最新的研究结果指出，异常表观遗传调控与SLE之间的关联，这引起了世界范围内的极大兴趣。本文就表观遗传学异常调控与SLE的关系，包括SLE患者DNA甲基化、组蛋白修饰和microRNA的改变，表观遗传学改变导致免疫功能障碍的可能机制，以及表观遗传学异常调控在SLE发生发展中的作用进行综述，并为SLE的相关治疗提供参考。
Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organs and the presence of anti-nuclear antibodies. The pathogenesis of SLE has been intensively studied but remains far from clear. B and T lymphocyte abnormalities, dysregulation of apoptosis, defects in the clearance of apoptotic materials, and various genetic and epigenetic factors are attributed to the development of SLE. The latest research findings point to the association between abnormal epigenetic regulation and SLE, which has attracted considerable interest worldwide. It is the purpose of this review to present and discuss the relationship between aberrant epigenetic regulation and SLE, including DNA methylation, histone modifications and microRNAs in patients with SLE, the possible mechanisms of immune dysfunction caused by epigenetic changes, and to better understand the roles of aberrant epigenetic regulation in the initiation and development of SLE and to provide an insight into the related therapeutic options in SLE.
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