The inflammation hypothesis and its potential relevance to statin therapy

被引：122

作者：

Forrester, James S. ^{[1
]}

Libby, Peter

机构：

[1] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA

[2] Harvard Univ, Sch Med, Boston, MA 02115 USA

[3] Brigham & Womens Hosp, Boston, MA 02115 USA

来源：

AMERICAN JOURNAL OF CARDIOLOGY | 2007年 / 99卷 / 05期

关键词：

D O I：

10.1016/j.amjcard.2006.09.125

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Inflammatory cytokines have a central role in atherogenesis and plaque rupture. These mediators, including tumor necrosis factor, interleukins, and matrix metalloproteinases and transforming growth factor-beta are also prominent in other chronic progressive diseases characterized by cell apoptosis and tissue fibrosis. This review extends the inflammation hypothesis to critical analysis of studies to bearing on the role of inflammation in chronic conditions that commonly accompany coronary disease. Because statins inhibit the expression of inflammatory mediators, the review then analyzes the laboratory and clinical data that may justify trials of statins in nonatherosclerotic disease. In conclusion, despite far different clinical presentations, chronic progressive diseases characterized by apoptosis and fibrosis have persistence of inflammatory cytokines as a final common pathway, and thus may benefit from the pleiotropic effects of statin therapy. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：732 / 738

页数：7

共 58 条

[1] Serum from patients with severe heart failure downregulates eNOS and is proapoptotic -: Role of tumor necrosis factor-α [J].