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

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.

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