Our study identifies a previously unknown proteolytic activity of PLA2 that is specific to apoA-I and may contribute to the enhanced catabolism of apoA-I in inflammation and atherosclerosis.
Consequently, our results indicate a potential role for both cytosolic and secretory PLA(2) enzymes in inflammation and in macrophage functions related to atherosclerosis, with a specific role for group IIa snpPLA2 in LDL scavenging.
The findings of this study suggest that Pl(A1/A1) homozygotes may be prone to early atherosclerosis and more rapid progression of stable CAD whereas carriers of the PlA2 allele are more prone to thrombotic complications.
The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk in patients with APS and preclinical arteriosclerosis in patients with SLE.