国际儿科学杂志
國際兒科學雜誌
국제인과학잡지
INTERNATIONAL JOURNAL OF PEDIATRICS
2014年
5期
538-541
,共4页
曾慧勤(综述)%张建江(审校)
曾慧勤(綜述)%張建江(審校)
증혜근(종술)%장건강(심교)
肾纤维化%表观遗传%DNA甲基化%组蛋白修饰
腎纖維化%錶觀遺傳%DNA甲基化%組蛋白脩飾
신섬유화%표관유전%DNA갑기화%조단백수식
Kidney fibrosis%Epigenetics%DNA methylation%Histone modification
表观遗传与人类健康及疾病息息相关,这种“第二套遗传密码”精密地控制着真核细胞的整个代谢过程。在表观遗传基因沉默/表达调控中,由DNA启动子区CpG岛过度甲基化/组蛋白修饰等原因导致的转录抑制是两种最常见的机制,特定基因如Ras蛋白激活物类似物-1的启动子区甲基化沉默导致的下游信号通路的异常激活与成纤维细胞异常增殖和肾纤维化密切相关。近年来,越来越多的证据表明表观遗传修饰可能在成纤维细胞的激活以及肾纤维化过程中发挥重要作用。该文就近期表观遗传修饰与慢性肾脏病尤其是肾纤维化的相关研究作一综述,以期为肾纤维化的发病机制研究及临床诊治提供新思路。
錶觀遺傳與人類健康及疾病息息相關,這種“第二套遺傳密碼”精密地控製著真覈細胞的整箇代謝過程。在錶觀遺傳基因沉默/錶達調控中,由DNA啟動子區CpG島過度甲基化/組蛋白脩飾等原因導緻的轉錄抑製是兩種最常見的機製,特定基因如Ras蛋白激活物類似物-1的啟動子區甲基化沉默導緻的下遊信號通路的異常激活與成纖維細胞異常增殖和腎纖維化密切相關。近年來,越來越多的證據錶明錶觀遺傳脩飾可能在成纖維細胞的激活以及腎纖維化過程中髮揮重要作用。該文就近期錶觀遺傳脩飾與慢性腎髒病尤其是腎纖維化的相關研究作一綜述,以期為腎纖維化的髮病機製研究及臨床診治提供新思路。
표관유전여인류건강급질병식식상관,저충“제이투유전밀마”정밀지공제착진핵세포적정개대사과정。재표관유전기인침묵/표체조공중,유DNA계동자구CpG도과도갑기화/조단백수식등원인도치적전록억제시량충최상견적궤제,특정기인여Ras단백격활물유사물-1적계동자구갑기화침묵도치적하유신호통로적이상격활여성섬유세포이상증식화신섬유화밀절상관。근년래,월래월다적증거표명표관유전수식가능재성섬유세포적격활이급신섬유화과정중발휘중요작용。해문취근기표관유전수식여만성신장병우기시신섬유화적상관연구작일종술,이기위신섬유화적발병궤제연구급림상진치제공신사로。
Epigenetics, which is called second genetic code precisely and controls the total metabolic processes of eukaryotic cells,has an inseparable correlation with human health and diseases. Among all the gene silencing mechanisms of epigenetic modifications,CpG islands of DNA promoter hypermethylation/histone mod-ifications are two major causes. Promoter methylation of specific genes,such as Ras protein activator analogue 1 may lead to aberrant activation of downstream signaling pathways,following by fibroblasts proliferation and kid-ney fibrosis. In recent years,epigenetic modifications have been proved to play a major role in preventing fibro-blasts to return to their quiescent stage,ultimately contributing to fibrosis in the kidney. This paper provides a glimpse of recent studies on epigenetic mechanisms of chronic kidney diseases,especially renal fibrosis,with an aim to provide new insights into pathogenesis research and clinical diagnosis and treatment.