title: Inflammatory cytokines and postmyocardial infarction remodeling.
abstract: 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.
authors.affiliation: Heart & Stroke/RL Centre of Excellence, NCSB11-1266, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, M5G 2C4, Canada.
authors.forename: Min
authors.initials: M
authors.lastname: Nian
authors.forename: Paul
authors.initials: P
authors.lastname: Lee
authors.forename: Neelam
authors.initials: N
authors.lastname: Khaper
authors.forename: Peter
authors.initials: P
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000209:etiology; D003094:Collagen / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000502:physiology*; D015195:Drug Design; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000502:physiology*; D016023:Integrins / Q000502:physiology; D051379:Mice; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D018919:Neovascularization, Physiologic; D018384:Oxidative Stress; D013314:Stress, Mechanical; D015291:Transforming Growth Factors / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D016023:Integrins; D015291:Transforming Growth Factors; D003094:Collagen