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首页> 外文期刊>Seminars in dialysis >Causes of dysregulation of lipid metabolism in chronic renal failure.
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Causes of dysregulation of lipid metabolism in chronic renal failure.

机译：慢性肾功能衰竭中脂质代谢失调的原因。

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摘要

End-stage renal disease (ESRD) is associated with accelerated atherosclerosis and premature death from cardiovascular disease. These events are driven by oxidative stress inflammation and lipid disorders. ESRD-induced lipid abnormalities primarily stem from dysregulation of high-density lipoprotein (HDL), triglyceride-rich lipoprotein metabolism, and oxidative modification of lipoproteins. In this context, production and plasma concentration of Apo-I and Apo-II are reduced, HDL maturation is impaired, HDL composition is altered, HDL antioxidant and anti-inflammatory functions are depressed, clearance of triglyceride-rich lipoproteins and their atherogenic remnants is impaired, their composition is altered, and their plasma concentration is elevated in ESRD. The associated defect in HDL maturation is largely caused by acquired lecithin-cholesterol acyltransferase deficiency while its triglyceride enrichment is due to hepatic lipase deficiency. Hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are mediated by down-regulation of lipoprotein lipase, hepatic lipase, very low-density lipoprotein (VLDL) receptor, and LDL receptor-related protein, relative reduction in ApoC-II/ApoC-III ratio, up-regulation of acyl-CoA cholesterol acyltransferase, and elevated plasma level of cholesterol ester-poor prebeta HDL. Impaired clearance and accumulation of oxidation-prone VLDL and chylomicron remnants and abnormal LDL composition in the face of oxidative stress and inflammation favors their uptake by macrophages and resident cells in the artery wall. The effect of heightened influx of lipids is compounded by impaired HDL-mediated reverse cholesterol transport leading to foam cell formation which is the central event in atherosclerosis plaque formation and subsequent plaque rupture, thrombosis, and tissue damage.
机译：终末期肾脏疾病（ESRD）与动脉粥样硬化的加速和心血管疾病的过早死亡有关。这些事件是由氧化应激炎症和脂质紊乱驱动的。 ESRD引起的脂质异常主要源于高密度脂蛋白（HDL）的调节失调，富含甘油三酸酯的脂蛋白代谢以及脂蛋白的氧化修饰。在这种情况下，Apo-I和Apo-II的产生和血浆浓度降低，HDL成熟受损，HDL组成改变，HDL抗氧化剂和抗炎功能下降，富含甘油三酸酯的脂蛋白及其动脉粥样硬化残留物的清除率降低。在ESRD中受损，其组成改变，血浆浓度升高。高密度脂蛋白成熟的相关缺陷主要是由于获得性卵磷脂-胆固醇酰基转移酶缺乏引起的，而甘油三酸酯的富集则是由于肝脂肪酶缺乏引起的。高甘油三酸酯血症，异常组成和富含甘油三酸酯的脂蛋白及其残余物清除率的降低是由脂蛋白脂酶，肝脂酶，极低密度脂蛋白（VLDL）受体和LDL受体相关蛋白的下调，ApoC相对减少引起的-II / ApoC-III比率，酰基辅酶A胆固醇酰基转移酶的上调和血浆胆固醇水平低的prebeta HDL的血浆水平升高。面对氧化应激和炎症，易氧化的VLDL和乳糜微粒残留物的清除和积累受损，LDL组成异常，有利于巨噬细胞和动脉壁中的驻留细胞摄取。 HDL介导的胆固醇逆向转运功能受损，导致泡沫细胞形成，这是动脉粥样硬化斑块形成以及随后斑块破裂，血栓形成和组织损伤的主要事件，从而加剧了脂质流入的影响。

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