Roxborough H E, Young I S
Department of Clinical Biochemistry, Queen's University of Belfast, Northern Ireland.
Med Hypotheses. 1995 Aug;45(2):125-8. doi: 10.1016/0306-9877(95)90059-4.
The incidence of atherosclerosis is greatly increased in patients with chronic renal failure, and this increased risk is only partly explained by conventional risk factors. Carbamylation of proteins occurs in renal failure as a result of reactions between urea-derived cyanate and protein amino groups. A mechanism is proposed whereby oxidation of LDL cholesterol within the arterial wall may be enhanced as a result of carbamylation. This may be accentuated as a result of inhibition of antioxidant enzymes by carbamylation. The combination of these processes may lead to increased atherogenesis.
慢性肾衰竭患者动脉粥样硬化的发病率大幅增加，而这种风险增加仅部分由传统风险因素解释。肾衰竭时，由于尿素衍生的氰酸盐与蛋白质氨基之间的反应，会发生蛋白质氨甲酰化。本文提出了一种机制，即氨甲酰化可能会增强动脉壁内低密度脂蛋白胆固醇的氧化。由于氨甲酰化对抗氧化酶的抑制作用，这种情况可能会加剧。这些过程的综合作用可能导致动脉粥样硬化的增加。
