表观遗传学
染色体易位
DNA甲基化
DNA去甲基化
染色质
5-羟甲基胞嘧啶
生物
肾
信使核糖核酸
表观基因组
抑制因子
5-甲基胞嘧啶
DNA
染色质重塑
基因
甲基化
遗传学
基因表达
作者
Qian Zhang,Jiahui Li,Li Tan,Jun Xue,Yujiang Geno Shi
出处
期刊:Biochemical Society Transactions
[Portland Press]
日期:2024-10-08
摘要
Epigenetic mechanisms play a critical role in the pathogenesis of human diseases including kidney disorders. As the erasers of DNA methylation, Ten-eleven translocation (TET) family proteins can oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC), thus leading to passive or active DNA demethylation. Similarly, TET family proteins can also catalyze the same reaction on RNA. In addition, TET family proteins can also regulate chromatin structure and gene expression in a catalytic activity-independent manner through recruiting the SIN3A/HDAC co-repressor complex. In 2012, we reported for the first time that the genomic 5-hydroxymethylcytosine level and the mRNA levels of Tet1 and Tet2 were significantly downregulated in murine kidneys upon ischemia and reperfusion injury. Since then, accumulating evidences have eventually established an indispensable role of TET family proteins in not only acute kidney injury but also chronic kidney disease. In this review, we summarize the upstream regulatory mechanisms and the pathophysiological role of TET family proteins in major types of kidney diseases and discuss their potential values in clinical diagnosis and treatment.
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