首页> 美国卫生研究院文献>Cells >MicroRNA-221: A Fine Tuner and Potential Biomarker of Chronic Liver Injury
【2h】

MicroRNA-221: A Fine Tuner and Potential Biomarker of Chronic Liver Injury

机译:microRNA-221:一种细调谐器和慢性肝损伤的潜在生物标志物

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The last decade has witnessed significant advancements in our understanding of how small noncoding RNAs, such as microRNAs (miRNAs), regulate disease progression. One such miRNA, miR-221, has been shown to play a key role in the progression of liver fibrosis, a common feature of most liver diseases. Many reports have demonstrated the upregulation of miR-221 in liver fibrosis caused by multiple etiologies such as viral infections and nonalcoholic steatohepatitis. Inhibition of miR-221 via different strategies has shown promising results in terms of the suppression of fibrogenic gene signatures in vitro, as well as in vivo, in independent mouse models of liver fibrosis. In addition, miR-221 has also been suggested as a noninvasive serum biomarker for liver fibrosis and cirrhosis. In this review, we discuss the biology of miR-221, its significance and use as a biomarker during progression of liver fibrosis, and finally, potential and robust approaches that can be utilized to suppress liver fibrosis via inhibition of miR-221.
机译:过去十年目睹了我们对非划分RNA(如MicroRNA(miRNA),调节疾病进展的小型rNA)的理解有重大进步。已经证明了一种这样的miRNA,miR-221,在肝纤维化进展中发挥关键作用,是大多数肝病的常见特征。许多报道证明了由多种病因如病毒感染和非酒精性脱脂性炎引起的肝纤维化中miR-221的上调。通过不同策略的MIR-221的抑制表明,在肝纤维化的独立小鼠模型中,在体外抑制纤维遗传基因签名的抑制方面具有有希望的结果。此外,MIR-221还提出作为肝纤维化和肝硬化的非血清血清生物标志物。在本综述中,我们讨论了MiR-221的生物学,其重要性和用作肝纤维化进展过程中的生物标志物,最后,可通过抑制miR-221来抑制肝纤维化的潜在和鲁棒方法。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号