Matrix-dependent perturbation of TGFβ signaling and disease

被引：105
作者：
Doyle, Jefferson J. [1 ,2 ]
Gerber, Elizabeth E. [1 ,2 ]
Dietz, Harry C. [1 ,2 ,3 ,4 ]
机构：
[1] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA
[2] Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Pediat Cardiol, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA
来源：
FEBS LETTERS | 2012年 / 586卷 / 14期
关键词：
Transforming growth factor beta; Extracellular matrix; Marfan syndrome; Stiff skin syndrome; Fibrillin; Integrin; GROWTH-FACTOR-BETA; SMOOTH-MUSCLE-CELLS; THORACIC AORTIC-ANEURYSM; HEREDITARY HEMORRHAGIC TELANGIECTASIA; WEILL-MARCHESANI-SYNDROME; RECEPTOR-TYPE-II; MARFAN-SYNDROME; ANGIOTENSIN-II; SYSTEMIC-SCLEROSIS; MOUSE MODEL;
D O I：
10.1016/j.febslet.2012.05.027
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Transforming growth factor beta (TGF beta) is a multipotent cytokine that is sequestered in the extracellular matrix (ECM) through interactions with a number of ECM proteins. The ECM serves to concentrate latent TGF beta at sites of intended function, to influence the bioavailability and/or function of TGF beta activators, and perhaps to regulate the intrinsic performance of cell surface effectors of TGF beta signal propagation. The downstream consequences of TGF beta signaling cascades in turn provide feedback modulation of the ECM. This review covers recent examples of how genetic mutations in constituents of the ECM or TGF beta signaling cascade result in altered ECM homeostasis, cellular performance and ultimately disease, with an emphasis on emerging therapeutic strategies that seek to capitalize on this refined mechanistic understanding. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码：2003 / 2015
页数：13
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