A primer on the epigenetics of kidney fibrosis

被引：0
|
作者：
Tampe, D. [1 ]
Zeisberg, M. [1 ]
机构：
[1] Univ Gottingen, Med Ctr, Dept Nephrol & Rheumatol, D-37075 Gottingen, Germany
来源：
MINERVA MEDICA | 2012年 / 103卷 / 04期
关键词：
Epigenesis; genetic; Kidney; Fibrosis; PHASE-II TRIAL; DEACETYLASE INHIBITOR BELINOSTAT; CISPLATIN PLUS DECITABINE; DNA-HYPOMETHYLATING AGENT; ACUTE MYELOID-LEUKEMIA; TRANS-RETINOIC ACID; SODIUM PHENYLBUTYRATE; VALPROIC ACID; FIBROBLAST ACTIVATION; CLINICAL-TRIAL;
D O I：
暂无
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Despite extensive knowledge of the various molecular pathways that contribute to tubulointerstitial fibrosis, it remains an unsolved question why the progression rate of chronic kidney disease varies substantially from patient to patient, even among patients with common underlying nephropathies and comorbidities. Possible explanations for different susceptibilities of individual patients to develop end-stage renal failure include genetic or epigenetic variations, which modify how individual patients respond to kidney injury. Here we review principles of epigenetic mechanisms in context of chronic kidney disease and discuss how such insights may be utilized for future therapeutic strategies and may lead to novel diagnostic tools in the future.
引用
收藏
页码：267 / 278
页数：12
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