TGF-β Signaling via TAK1 Pathway: Role in Kidney Fibrosis

被引：125
作者：
Choi, Mary E. [1 ]
Ding, Yan [1 ]
Kim, Sung Il [1 ]
机构：
[1] Harvard Univ, Sch Med, Div Renal, Brigham & Womens Hosp,Dept Med, 4 Blackfan Circle,HIM-5, Boston, MA 02115 USA
来源：
SEMINARS IN NEPHROLOGY | 2012年 / 32卷 / 03期
基金：
美国国家卫生研究院;
关键词：
Transforming growth factor-beta 1; intracellular signaling; TGF-beta-activated kinase 1; fibrosis; chronic kidney disease; GROWTH-FACTOR-BETA; PROTEIN-KINASE ACTIVATION; TRANSFORMING GROWTH-FACTOR-BETA-1; KAPPA-B; P38; MAPK; PHOSPHATIDYLINOSITOL; 3-KINASE; INFLAMMATORY RESPONSE; FIBRONECTIN SYNTHESIS; DEPENDENT ACTIVATION; TARGETED DISRUPTION;
D O I：
10.1016/j.semnephrol.2012.04.003
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
In progressive kidney diseases, fibrosis represents the common pathway to end-stage kidney failure. Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic cytokine that has been established as a central mediator of kidney fibrosis. Emerging evidence shows a complex scheme of signaling networks that enable multifunctionality of TGF-beta 1 actions. Specific targeting of the TGF-beta signaling pathway is seemingly critical and an attractive molecular therapeutic strategy. TGF-beta 1 signals through the interaction of type I and type II receptors to activate distinct intracellular pathways involving the Smad and the non-Smad. The Smad signaling axis is known as the canonical pathway induced by TGF-beta 1. Importantly, recent investigations have shown that TGF-beta 1 also induces various non-Smad signaling pathways. In this review, we focus on current insights into the mechanism and function of the Smad-independent signaling pathway via TGF-beta-activated kinase 1 and its role in mediating the profibrotic effects of TGF-beta 1. Semin Nephrol 32:244-252 (c) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：244 / 252
页数：9
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