The role of the Janus kinase family/signal transducer and activator of transcription signaling pathway in fibrotic renal disease.

The role of the Janus kinase family/signal transducer and activator of transcription signaling pathway in fibrotic renal disease.
复制标题

Janus激酶家族/信号换能器和转录信号通路激活因子在纤维化肾脏疾病中的作用。

DOI:
10.1016/j.jss.2012.06.050
复制
发表时间:
2012-11
期刊:
The Journal of surgical research
影响因子:
--
通讯作者:
Meldrum KK
Meldrum KK
中科院分区:
其他
文献类型:
--
作者:
Matsui F;Meldrum KK

文献摘要

被引文献

相似文献

在过去的几年中,许多细胞因子和生长因子,包括转化生长因子β1、肿瘤坏死因子α和血管紧张素II已被证明在肾纤维化中发挥着至关重要的作用。 Janus激酶家族(JAK)和信号转导和转录激活因子(STAT)构成调节细胞因子表达的主要信号通路之一,并且JAK/STAT信号通路越来越多地与肾脏疾病的病理生理学相关。本综述探讨了 JAK/STAT 信号通路在纤维化肾病中的作用。 JAK/STAT 信号通路在多种肾脏疾病中被激活,并与肾纤维化的病理生理学有关。实验证据表明,抑制 JAK/STAT 信号通路,特别是 JAK2 和 STAT3,可以抑制肾纤维化并保护肾功能。然而,目前尚不完全清楚哪些细胞激活JAK/STAT信号通路以及每种肾脏疾病中哪些JAK/STAT信号通路被激活。关于 JAK/STAT 信号传导及其对肾脏疾病的影响的研究仍在人类中进行。未来的研究需要阐明 JAK/STAT 信号传导抑制作为减轻肾纤维化的治疗策略的潜在作用。
Over the past several years, a number of cytokines and growth factors including transforming growth factor β1, tumor necrosis factor α, and angiotensin II have been shown to play a crucial role in renal fibrosis. The Janus kinase family (JAK) and signal transducers and activators of transcription (STATs) constitute one of the primary signaling pathways that regulate cytokine expression, and the JAK/STAT signaling pathway has increasingly been implicated in the pathophysiology of renal disease. This review examines the role of the JAK/STAT signaling pathway in fibrotic renal disease. The JAK/STAT signaling pathway is activated in a variety of renal diseases and has been implicated in the pathophysiology of renal fibrosis. Experimental evidence suggests that inhibition of the JAK/STAT signaling pathway, in particular JAK2 and STAT3, may suppress renal fibrosis and protect renal function. However, it is incompletely understood which cells activate the JAK/STAT signaling pathway and which JAK/STAT signaling pathway is activated in each renal disease. Research regarding JAK/STAT signaling and its contribution to renal disease is still ongoing in humans. Future studies are required to elucidate the potential role of JAK/STAT signaling inhibition as a therapeutic strategy in the attenuation of renal fibrosis.