Circulation Research. 2004;94:1543-1553
doi: 10.1161/01.RES.0000130526.20854.fa
doi: 10.1161/01.RES.0000130526.20854.fa
© 2004 American Heart Association, Inc.
Reviews |
Inflammatory Cytokines and Postmyocardial Infarction Remodeling
From Heart & Stroke/Richard Lewar Centre of Excellence, University of Toronto; and Division of Cardiology, Toronto General Hospital, University Health Network, Toronto, Canada.
Correspondence to Dr. Peter Liu, Heart & Stroke/RL Centre of Excellence, NCSB11-1266, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, M5G 2C4, Canada. E-mail peter.liu{at}utoronto.ca
This Review is part of a thematic series on Chemokines and Cytokines, which includes the following articles:
Inflammatory Mediators and the Failing Heart: Past, Present and the Foreseeable Future
Inflammatory Cytokines and Postmyocardial Infarction Remodeling
Cytokines in Ventricular Function
Chemokines/Cytokines
Peter Liu Guest Editor
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.
Key Words: remodeling • cytokines • inflammation • myocardial infarction • matrix • integrins
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