Mechanism of cardiac fibrosis by angiotensin - New insight revealed by genetic engineering

被引：15

作者：

Matsusaka, T ^{[1
]}

Katori, H

Homma, T

Ichikawa, I

机构：

[1] Tokai Univ, Inst Med Sci Mol & Cellular Nephrol, Isehara, Kanagawa 2591193, Japan

[2] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37212 USA

[3] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA

[4] Tokai Univ, Dept Pediat, Kanagawa 2591100, Japan

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 1999年 / 9卷 / 07期

关键词：

D O I：

10.1016/S1050-1738(00)00018-9

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Accumulating data show that excess of angiotensin II (Ang II) is involved in cardiac fibrosis. Many experimental studies suggested that Ang II induces cardiac fibrosis not by its blood pressure-raising action, but rather by a direct action on the heart. However, it has been difficult to distinguish the local and systemic actions in vivo. Recent generic technology sheds new light on this problem. This review focuses on the recent advances and newly arising issues regarding the mechanism of Ang II-induced cardiac fibrosis. (Trends Cardiovasc Med 1999;9:180-184). (C) 1999, Elsevier Science Inc.

引用

页码：180 / 184

页数：5

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