Inhibition of sPLA2-IIA, C-reactive Protein or Complement: New Therapy for Patients with Acute Myocardial Infarction?

Author(s): Paul A.J. Krijnen, Christof Meischl, Remco Nijmeijer, Cees A. Visser, C. Erik Hack, Hans W.M. Niessen

Journal Name: Cardiovascular & Hematological Disorders-Drug Targets
Formerly Current Drug Targets - Cardiovascular & Hematological Disorders

Volume 6 , Issue 2 , 2006

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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

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Article Details

Year: 2006
Published on: 01 March, 2012
Page: [111 - 121]
Pages: 11
DOI: 10.2174/187152906777441830
Price: $65

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