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Cardiovascular Research 2003 60(1):68-77; doi:10.1016/S0008-6363(03)00324-9
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Type II secretory phospholipase A2 in cardiovascular disease: a mediator in atherosclerosis and ischemic damage to cardiomyocytes?

Hans W.M Niessena,b,*,1, Paul A.J Krijnena,b,1, Cees A Vissera,c, Chris J.L.M Meijerb and C Erik Hacka,d,e

aICaR-VU, VU Medical Center, Amsterdam, The Netherlands
bDepartment of Pathology, VU Medical Center, Amsterdam, The Netherlands
cDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands
dDepartment of Clinical Chemistry, VU Medical Center, Amsterdam, The Netherlands
eDepartment of Immunopathology, Sanquin Research at CLB, Amsterdam, The Netherlands

*Corresponding author. VU Medical Center, Department of Pathology, Room nr. OE16, De Boelelaan 1117, 1007 MB Amsterdam, The Netherlands. Tel.: +31-20-444-4003; fax: +31-20-444-2964. Email address: jwm.niessen{at}vumc.nl

Inflammatory reactions contribute to the pathogenesis of cardiovascular conditions such as atherosclerosis and ischemic damage in acute myocardial infarction (AMI). Among the mediators involved in inflammation are secretory phospholipase A2 group II (sPLA2-II) enzymes. Though some cells constitutively express sPLA2-II, the synthesis by cells such as hepatocytes is typical for an acute-phase reactant. Recent literature suggests multiple roles for sPLA2-II in cardiovascular disease. In this review we discuss the role of sPLA2-II in various in vivo and in vitro models of atherosclerosis or AMI, including the therapeutic perspective of sPLA2-II inhibitors. It was concluded that sPLA2-II appears to be an important inflammatory mediator of cardiovascular disease.

KEYWORDS Phospholipases; Ischemia; Infection/inflammation; Artherosclerosis

1 Hans Niessen and Paul Krijnen contributed equally to this review.

Time for primary review 28 days.


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