The role of Smad3-dependent TGF-β signal in vascular response to injury

被引：21

作者：

Yokote, Koutaro ^{[1
]}

Kobayashi, Kazuki ^{[1
]}

Saito, Yasushi ^{[1
]}

机构：

[1] Chiba Univ Hosp, Div Endocrinol Diabet & Metab, Dept Internal Med, Chuo Ku, Chiba 260, Japan

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2006年 / 16卷 / 07期

关键词：

D O I：

10.1016/j.tcm.2006.04.005

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Transforming growth factor (TGF)-beta is a multifunctional cytokine involved in the regulation of proliferation, differentiation, migration, and survival of many different cell types. The role of TGF-beta in atherosclerosis has been intensively studied, but the precise function of the downstream signals in this disease entity remains unclear. We recently discovered that mice lacking Smad3, a major downstream mediator of TGF-beta, show enhanced neointimal hyperplasia with decreased matrix deposition in response to vascular injury. This review summarizes the current view on involvement of TGF-beta in atherosclerotic vascular disease and discusses the role of Smad3-dependent TGF-beta signal in vascular response to injury.

引用

页码：240 / 245

页数：6

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