Inflammatory cytokines and postmyocardial infarction remodeling

被引:908
作者
Nian, M
Lee, P
Khaper, N
Liu, P
机构
[1] Univ Toronto, Heart & Stroke Richard Lewar Ctr Excellence, Toronto, ON, Canada
[2] Univ Hlth Network, Toronto Gen Hosp, Div Cardiol, Toronto, ON, Canada
关键词
remodeling cytokines; inflammation; myocardial infarction; matrix; integrins;
D O I
10.1161/01.RES.0000130526.20854.fa
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Inflammatory response and cytokine elaboration are particularly active after myocardial infarction and contribute to cardiac remodeling and eventual host outcome. The triggers of cytokine release in the acute postinfarction period include mechanical deformation, ischemic stimulus, reactive oxygen species (ROS), and cytokine self-amplification pathways. Acutely, the elaboration of tumor necrosis factor, IL-1 and IL-6, transforming growth factor families of cytokines, contribute to survival or deaths of myocytes, modulation of cardiac contractility, alterations of vascular endothelium, and recruitment of additional circulating cells of inflammation to the injured myocardium. This leads to further local oxidative stress and remodeling but also initiates the processes of wound healing. Chronically, sustained presence of cytokines leads to myocyte phenotype transition and activation of matrix metalloproteinases that modifies interstitial matrix, augmenting further the remodeling process. This in turn alters the local collagen composition and also the integrins that constitute the interface between myocytes and the matrix. These processes ultimately, when favorable, pave the way for angiogenesis and cellular regeneration. Thus, the insightful modulation of cytokines through current and future therapies could promote improved healing and cardiac remodeling postmyocardial infarction.
引用
收藏
页码:1543 / 1553
页数:11
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