Glycerophospholipids represent a common class of lipids critically important for integrity of cellular membranes. Oxidation of esterified unsaturated fatty acids dramatically changes biological activities of phospholipids. Apart from impairment of their structural function, oxidation makes oxidized phospholipids (OxPLs) markers of "modified-self" type that are recognized by soluble and cell-associated receptors of innate immunity, including scavenger receptors, natural (germ line-encoded) antibodies, and C-reactive protein, thus directing removal of senescent and apoptotic cells or oxidized lipoproteins. In addition, OxPLs acquire novel biological activities not characteristic of their unoxidized precursors, including the ability to regulate innate and adaptive immune responses. Effects of OxPLs described in vitro and in vivo suggest their potential relevance in different pathologies, including atherosclerosis, acute inflammation, lung injury, and many other conditions. This review summarizes current knowledge on the mechanisms of formation, structures, and biological activities of OxPLs. Furthermore, potential applications of OxPLs as disease biomarkers, as well as experimental therapies targeting OxPLs, are described, providing a broad overview of an emerging class of lipid mediators.

A comprehensive and standardized system to report lipid structures analyzed by mass spectrometry is essential for the communication and storage of lipidomics data. Herein, an update on both the LIPID MAPS classification system and shorthand notation of lipid structures is presented for lipid categories Fatty Acyls (FA), Glycerolipids (GL), Glycerophospholipids (GP), Sphingolipids (SP), and Sterols (ST). With its major changes, i.e. annotation of ring double bond equivalents and number of oxygens, the updated shorthand notation facilitates reporting of newly delineated oxygenated lipid species as well. For standardized reporting in lipidomics, the hierarchical architecture of shorthand notation reflects the diverse structural resolution powers provided by mass spectrometric assays. Moreover, shorthand notation is expanded beyond mammalian phyla to lipids from plant and yeast phyla. Finally, annotation of atoms is included for the use of stable isotope-labelled compounds in metabolic labelling experiments or as internal standards.This update on lipid classification, nomenclature and shorthand annotation for lipid mass spectra is considered a standard for lipid data presentation.

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Abstract-Angiogenesis is a common feature observed in advanced atherosclerotic lesions. We hypothesized that oxidized phospholipids (OxPLs), which accumulate in atherosclerotic vessels can stimulate angiogenesis. We found that oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) stimulated the formation of sprouts from endothelial cell spheroids and promoted growth of capillaries into Matrigel plugs in mice. OxPLs stimulated expression of vascular endothelial growth factor (VEGF) in vivo and in several normal and tumor cell types in vitro. Key Words: oxidized phospholipids Ⅲ atherosclerosis Ⅲ angiogenesis Ⅲ plaque destabilization T he adventitial layer of human coronary arteries contains a network of microvasculature, termed vasa vasorum, that delivers oxygen and nutrients to the outer layers of the arterial wall. In contrast to the adventitia, the intima and the inner media of normal large arteries usually do not contain capillaries. However, during atherosclerotic plaque formation, microvessels appear in the thickened intima and media of more that 40% of lesions. 1,2 These neovessels originate mainly from the adventitial vasa vasorum and support growth of atherosclerotic intima beyond the critical thickness limited by diffusion from the major arterial lumen. 3 It has been widely hypothesized that neovascularization is a causative factor for atherosclerotic plaque growth and destabilization. Although these issues are difficult to address in a direct experiment (discussed in Khurana et al 4 ), there is much indirect evidence suggesting that neovascularization can influence the evolution of atheroma via several mechanisms. The density of vasa vasorum strongly correlates with the number of infiltrating mononuclear cells, suggesting that neovessels are an important route for the entry of leukocytes into advanced lesions. 2,5 Furthermore, intraplaque microvascular hemorrhages provide blood cell-derived lipids that deposit in the lipid core. 6,7 Microvessels are functionally important in atherogenesis as illustrated by the ability of angiogenesis inhibitors angiostatin and TNP-470 to reduce angiogenesis and inhibit the development of lesions in apoE knockout mice. 5,8 In contrast, angiogenic stimuli such as vascular endothelial growth factor (VEGF) promote lesion development. 9 Such data strongly suggest that formation of vasa vasorum stimulates the progression of atherosclerotic lesions.In addition to a role in plaque growth, the formation of neovessels potentially can decrease the stability of atheroma because of digestion of plaque tissue by metalloproteases secreted by growing capillaries. Indeed, unstable and ruptured atherosclerotic plaques are characterized by an increased density of plaque microvessels. 10,11 Hypoxia is among the strongest known angiogenic stimuli also thought to play a role in the development of intimal neovascularization. 12 However, additional microenvironmental factors independent of lesion thickness may also be important for plaque angiogenesis. In apoE-deficient mice,