Rader Daniel J, Puré Ellen
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Cell Metab. 2005 Apr;1(4):223-30. doi: 10.1016/j.cmet.2005.03.005.
Atherogenesis requires and is highly influenced by the interaction between lipoproteins and macrophages. Most of the focus to date has been on the ability of atherogenic lipoproteins (such as low-density lipoproteins, LDL) to promote and of anti-atherogenic lipoproteins (such as high-density lipoproteins, HDL) to prevent the development of the cholesteryl ester-enriched macrophage-derived foam cell. However, lipoprotein-macrophage interactions have the potential to modulate macrophage function in a variety of additional ways that may impact on atherosclerosis. These include modulating cellular cholesterol and oxysterol content, providing fatty acids as ligands for PPARs, and acting as ligands for macrophage scavenger and Toll-like receptors. We suggest that atherogenic lipoproteins promote and anti-atherogenic lipoproteins inhibit atherogenesis by modulating macrophage function in a variety of ways beyond cholesteryl ester accumulation and foam cell formation.
动脉粥样硬化的发生需要脂蛋白与巨噬细胞之间的相互作用，并且受到这种相互作用的高度影响。迄今为止，大多数研究重点都集中在致动脉粥样硬化脂蛋白（如低密度脂蛋白，LDL）促进以及抗动脉粥样硬化脂蛋白（如高密度脂蛋白，HDL）预防富含胆固醇酯的巨噬细胞源性泡沫细胞形成的能力上。然而，脂蛋白-巨噬细胞相互作用有可能通过多种其他方式调节巨噬细胞功能，而这些方式可能会影响动脉粥样硬化。这些方式包括调节细胞胆固醇和氧化甾醇含量、提供脂肪酸作为过氧化物酶体增殖物激活受体（PPARs）的配体，以及作为巨噬细胞清道夫受体和Toll样受体的配体。我们认为，致动脉粥样硬化脂蛋白通过多种方式调节巨噬细胞功能来促进动脉粥样硬化，而抗动脉粥样硬化脂蛋白则通过这些方式抑制动脉粥样硬化，这些方式不仅仅局限于胆固醇酯积累和泡沫细胞形成。
