脂蛋白相关磷脂酶A2
血小板活化因子
炎症
磷脂酶A2
磷脂
酶
医学
下调和上调
内科学
脂蛋白
内分泌学
脂质信号
磷脂酶
磷脂酶A
免疫学
花生四烯酸
生物化学
胆固醇
生物
基因
膜
标识
DOI:10.1007/s10557-008-6133-8
摘要
This article is focused on platelet-activating factor acetylhydrolase (PAF-AH), a lipoprotein bound, calcium-independent phospholipase A2 activity also referred to as lipoprotein-associated phospholipase A2 or PLA2G7. PAF-AH catalyzes the removal of the acyl group at the sn-2 position of PAF and truncated phospholipids generated in settings of inflammation and oxidant stress. Here, I discuss current knowledge related to the structural features of this enzyme, including the molecular basis for association with lipoproteins and susceptibility to oxidative inactivation. The circulating form of PAF-AH is constitutively active and its expression is upregulated by mediators of inflammation at the transcriptional level. This mechanism is likely responsible for the observed up-regulation of PAF-AH during atherosclerosis and suggests that increased expression of this enzyme is a physiological response to inflammatory stimuli. Administration of recombinant forms of PAF-AH attenuate inflammation in a variety of experimental models. Conversely, genetic deficiency of PAF-AH in defined human populations increases the severity of atherosclerosis and other syndromes. Recent advances pointing to an interplay among oxidized phospholipid substrates, Lp(a), and PAF-AH could hold the key to a number of unanswered questions.
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