Loss of Smad3 modulates wound healing

被引：73

作者：

Ashcroft, GS ^{[1
]}

Roberts, AB ^{[1
]}

机构：

[1] NCI, Lab Cell Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA

来源：

CYTOKINE & GROWTH FACTOR REVIEWS | 2000年 / 11卷 / 1-2期

关键词：

SMAD; TGF-beta signaling; wound healing; inflammation;

D O I：

10.1016/S1359-6101(99)00036-2

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：

TGF-beta plays a central and critical role in tissue repair. The recent identification of TGF-beta signal transduction pathways involving Smad proteins has now made it possible to explore their contribution to the activities of TGF-beta in vivo. Both Smad3 and its closely related homolog Smad2 act as latent nuclear transcriptional activators and mediate intracellular signaling by TGF-beta s and activin, each of which regulates cellular functions pivotal to cutaneous wound healing. Mice null for Smad3 (Smad3(ex8/ex8)) survive into adulthood and show accelerated cutaneous wound healing characterized by an increased rate of re-epithalialization and a reduced local inflammatory infiltrate. These data implicate Smad3 in specific pathways of tissue repair and suggest that it could be a target for the development of therapeutic strategies to modulate wound healing. Published by Elsevier Science Ltd.

引用

页码：125 / 131

页数：7

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