ApoA-I is a major protein component of high-density lipoprotein (HDL) that is widely known for regulating cholesterol trafficking and inflammatory and immune responses and for protecting against atherosclerosis. ApoA-I is generally considered to be synthesized in the liver (hepatocytes) and small intestine (enterocytes). However, computer analysis of ApoA-I has shown that the ApoA-I gene may be expressed in not only hepatocytes and enterocytes but also monocyte-macrophage cells, dendritic cells (DCs) and T cells. ApoA-I expression has been detected in THP-1 monocytes and macrophages, peripheral blood mononuclear cells (PBMCs) from postmenopausal women, human PBMC-derived monocytes and macrophages, mouse peritoneal macrophages, etc. Endogenous ApoA-I in macrophages has anti-inflammatory and cholesterol efflux effects. However, our understanding of the detailed roles of macrophage-synthesized ApoA-I is still at an early stage and very limited. More experiments are needed to elucidate the exact roles of endogenous ApoA-I in macrophages. Several lines of evidence indicate that recombinant exogenous human ApoA-I in mouse macrophages increases cholesterol efflux and thus reduces atherosclerosis development. Considering the antiatherogenic effect of exogenous ApoA-I overexpression in mouse macrophages, better understanding the role and mechanisms underlying macrophage-synthesized ApoA-I in atherosclerosis will enable macrophage-synthesized ApoA-I therapy to open new avenues for reducing the risk of atherosclerosis.

中文翻译：

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巨噬细胞中的内源性ApoA-I表达：预防动脉粥样硬化的潜在目标。

ApoA-I是高密度脂蛋白（HDL）的主要蛋白质成分，众所周知，它可调节胆固醇的运输，炎症和免疫反应以及预防动脉粥样硬化。通常认为ApoA-I是在肝脏（肝细胞）和小肠（肠细胞）中合成的。然而，对ApoA-1的计算机分析表明，ApoA-1基因不仅可以在肝细胞和肠细胞中表达，而且可以在单核巨噬细胞，树突状细胞（DC）和T细胞中表达。已在THP-1单核细胞和巨噬细胞，绝经后妇女的外周血单核细胞（PBMC），人PBMC衍生的单核细胞和巨噬细胞，小鼠腹膜巨噬细胞等中检测到ApoA-I表达。巨噬细胞中的内源性ApoA-I具有抗炎作用和胆固醇外流作用。然而，我们对巨噬细胞合成的ApoA-I的详细作用的了解仍处于早期阶段，并且非常有限。需要更多的实验来阐明内源性ApoA-I在巨噬细胞中的确切作用。几条证据表明，小鼠巨噬细胞中的重组外源人ApoA-I可增加胆固醇外流，从而减少动脉粥样硬化的发展。考虑到外源性ApoA-I在小鼠巨噬细胞中过度表达的抗动脉粥样硬化作用，更好地了解巨噬细胞合成的ApoA-I在动脉粥样硬化中的作用和机制将使巨噬细胞合成的ApoA-I治疗能够为减少动脉粥样硬化风险开辟新途径。需要更多的实验来阐明内源性ApoA-I在巨噬细胞中的确切作用。几条证据表明，小鼠巨噬细胞中的重组外源人ApoA-I可增加胆固醇外流，从而减少动脉粥样硬化的发展。考虑到外源性ApoA-I在小鼠巨噬细胞中过度表达的抗动脉粥样硬化作用，更好地了解巨噬细胞合成的ApoA-I在动脉粥样硬化中的作用和机制将使巨噬细胞合成的ApoA-I治疗能够为减少动脉粥样硬化风险开辟新途径。需要更多的实验来阐明内源性ApoA-I在巨噬细胞中的确切作用。几条证据表明，小鼠巨噬细胞中的重组外源人ApoA-I可增加胆固醇外流，从而减少动脉粥样硬化的发展。考虑到外源性ApoA-I在小鼠巨噬细胞中过度表达的抗动脉粥样硬化作用，更好地了解巨噬细胞合成的ApoA-I在动脉粥样硬化中的作用和机制将使巨噬细胞合成的ApoA-I治疗能够为减少动脉粥样硬化风险开辟新途径。