作者: Janne Oestvang , Berit Johansen
DOI: 10.1016/J.BBALIP.2006.06.003
关键词: Inflammation 、 Lysophospholipids 、 Phospholipase A 、 Lysophosphatidylcholine 、 Intracellular 、 Extracellular matrix 、 Lipid signaling 、 Biology 、 Cell biology 、 Biochemistry 、 Fibrosis
摘要: Abstract Atherosclerosis is a progressive inflammatory disease that takes place in the intima of arterial wall. It characterized by activation endothelial cells, proliferation smooth muscle cells and macrophages, accumulation lipoproteins, deposition extracellular matrix components enhanced lipolytic enzyme activity. Phospholipase A 2 (PLA ) has been postulated to play an important role process atherosclerosis, but its molecular mechanism uncertain. The secretory PLA expressed at increased levels atherosclerotic plaque may hydrolyze low-density lipoproteins (LDL). This action promotes production pro-inflammatory lipids such as lysophospholipids, unsaturated fatty acids eicosanoids. current review highlights recent findings on how LDL-derived lipid mediators, generated sPLA_2 modification LDL, regulate intracellular signaling macrophages. Moreover, discusses PLA_2 enzymes signalling collagen fibrotic development. could therefore function connector between inflammation fibrosis, latter being endpoint chronic inflammation.