Abstract
Reperfusion of ischemic myocardium after acute myocardial infarction (AMI) induces a local activation of inflammatory reactions that results in ischemia/reperfusion (I/R)-injury. I/R-injury contributes considerably to the total cell damage in the heart after AMI. Secretory phospolipase A2-IIA (sPLA2-IIA), C-reactive protein (CRP) and complement are inflammatory mediators that have been demonstrated to play key roles in I/R injury. From studies by us and others a mechanism emerged in which sPLA2-IIA binds to reversibly damaged cardiomyocytes and subsequently induces cell death, partly by potentiating binding of CRP and subsequent complement activation. Next to this, sPLA2-IIA also has a direct toxic effect, independent of CRP or complement. Therefore, these studies indicate a crucial role of inflammatory mediators in ischemia/reperfusion injury. This review will focus on the pathogenic effects of sPLA2-IIA, CRP and complement and on the putative therapeutic effects of inhibitors of these inflammatory mediators in acute myocardial infarction.
Keywords: inflammation, reperfused myocardium, Polymorphonuclear neutrophils (PMN), complement system, ischemia
Cardiovascular & Hematological Disorders-Drug Targets
Title: Inhibition of sPLA2-IIA, C-reactive Protein or Complement: New Therapy for Patients with Acute Myocardial Infarction?
Volume: 6 Issue: 2
Author(s): Paul A.J. Krijnen, Christof Meischl, Remco Nijmeijer, Cees A. Visser, C. Erik Hack and Hans W.M. Niessen
Affiliation:
Keywords: inflammation, reperfused myocardium, Polymorphonuclear neutrophils (PMN), complement system, ischemia
Abstract: Reperfusion of ischemic myocardium after acute myocardial infarction (AMI) induces a local activation of inflammatory reactions that results in ischemia/reperfusion (I/R)-injury. I/R-injury contributes considerably to the total cell damage in the heart after AMI. Secretory phospolipase A2-IIA (sPLA2-IIA), C-reactive protein (CRP) and complement are inflammatory mediators that have been demonstrated to play key roles in I/R injury. From studies by us and others a mechanism emerged in which sPLA2-IIA binds to reversibly damaged cardiomyocytes and subsequently induces cell death, partly by potentiating binding of CRP and subsequent complement activation. Next to this, sPLA2-IIA also has a direct toxic effect, independent of CRP or complement. Therefore, these studies indicate a crucial role of inflammatory mediators in ischemia/reperfusion injury. This review will focus on the pathogenic effects of sPLA2-IIA, CRP and complement and on the putative therapeutic effects of inhibitors of these inflammatory mediators in acute myocardial infarction.
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Cite this article as:
Krijnen A.J. Paul, Meischl Christof, Nijmeijer Remco, Visser A. Cees, Hack Erik C. and Niessen W.M. Hans, Inhibition of sPLA2-IIA, C-reactive Protein or Complement: New Therapy for Patients with Acute Myocardial Infarction?, Cardiovascular & Hematological Disorders-Drug Targets 2006; 6 (2) . https://dx.doi.org/10.2174/187152906777441830
DOI https://dx.doi.org/10.2174/187152906777441830 |
Print ISSN 1871-529X |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-4063 |
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