title: Ischemia and reperfusion related myocardial inflammation: A network of cells and mediators targeting the cardiomyocyte.
abstract: Occlusion of a coronary artery if maintained for longer period of time results in damage of the cardiac tissue. However, restoration of blood flow to previously ischemic tissue can itself induce further cardiac damage, a phenomenon known as myocardial reperfusion injury. Cardiac homoeostasis is supported by a network of direct and indirect interactions between cardiomyocytes and resident cell types such as fibroblasts, adipocytes, and endothelial cells or invading blood cells. This review will discuss the role of the cellular interplay in ischemia-reperfusion injury from a cardiomyocyte-centered view, although we are aware that other cellular interactions are equally important. We will try to work out currently unresolved questions and potential future directions in the field.
authors: Institute of Physiology, Justus Liebig University Giessen, Giessen, Germany.
authors: Susanne
authors: S
authors: Rohrbach
authors: Christian
authors: C
authors: Troidl
authors: Christian
authors: C
authors: Hamm
authors: Rainer
authors: R
authors: Schulz
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000473:pathology; D054392:Adipokines / Q000378:metabolism; D000818:Animals; D002450:Cell Communication; D003094:Collagen / Q000235:genetics; D016207:Cytokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D009205:Myocarditis / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009765:Obesity / Q000378:metabolism; D018384:Oxidative Stress
chemical_list: D054392:Adipokines; D016207:Cytokines; D003094:Collagen
keywords: cell death; collagen gene expression; disease models; oxidative stress; signal transduction