This a fascinating further insight into the complexities of the atherosclerotic process. How this relates to nutrition I do not know, but the interesting thought is what happens when the essential fatty acids are reduced in the diet. Which is a further aspect of this intriguing process.
Secretory phospholipase A, (sPLA,) enzymes hydrolyse the ester bond of phospholipid molecules at the sn-2 position to produce two potentially bioactive lipids that include non-esterified fatty acids (mainly arachidonic acid) and lysophospholipids. Of the ten-member family of sPLA, enzymes, groups IIA (sPLA,-IIA), V (sPLA,-V), and X (sPLA,-X) are highly expressed in human atherosclerotic lesions in which the various groups contribute differentially to atherogenesis.
Human A2 phospholipases (PLA2s) propagate inflammation by producing arachidonic acid precursors from membrane glycerophospholipid. Classes. Two of the five major PLA2 have been suggested to be involved in the atherosclerosis process and its complications: secretory type and lipoprotein-associated.
Population studies demonstrate the independent predictive value of increased circulating secretory PLA2 (sPLA2) and lipoprotein-associated PLA2 to predict the possibility of future cardiovascular disease events. PLAs are also aetiological risk factors for plaque progression, destabilisation, and rupture.
Three sPLA, subtypes are involved in the remodelling of lipoproteins, with adverse consequences for their function. sPLA,-X and sPLA,-V modify HDL, resulting in attenuation of its ability to affect reverse-cholesterol transport. sPLA,-lla and sPLA,-V remove phospholipids from LDL, making it more susceptible to retention through binding to matrix proteoglycans in the subintimal space. Consequently LDL is liable to increased oxidation, further increasing its affinity as a substrate for lipoprotein-associated PLA,. The products of lipoprotein-associated PLA, hydrolysis of oxidised LDL, Iysophosphatidylcholine and oxidised free fatty acids, have multiple proatherogenic actions, the most important being to increase apoptosis of macrophages in the necrotic core of vulnerable plaques, which predisposes the individual to rupture and coronary or cerebral thrombosis.
Corson 2009 Phospholipase A2, inhibitors in atherosclerosis: the race is on. Lancet , vol 373, pp 608-10
Rosenson et al 2009 Effects of 1-H-indole-3-glyoxamide (A-002) on concentrations of secretory phospholipase A2 ( plasma study ):a phase 11 doble bind, randomised, placebo-controlled trial . The Lancet vol 373 pp 649-58

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