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[脂蛋白(a):血栓形成与动脉粥样硬化之间的联系?]

[Lipoprotein(a): a link between thrombosis and atherosclerosis?].

作者信息

Hansen P R

机构信息

Rigshospitalet medicinsk afdeling B, København.

出版信息

Ugeskr Laeger. 1993 May 17;155(20):1527-30.

PMID:8316983
Abstract

Lipoprotein(a) (Lp(a)) represents a class of plasma lipoproteins similar to low-density lipoprotein (LDL), but containing an unique apolipoprotein(a) with striking homology to plasminogen. Plasma Lp(a) is inherited as a quantitative genetic trait, with a continuous distribution in Caucasian populations (< 10-2000 mg/l), where high levels are associated with an increased risk of atherosclerotic disease. The physiological role of Lp(a) is unknown, and the metabolism is obscure. Plasma Lp(a) is apparently resistent to diets and drug therapy, and LDL-apheresis is currently the most effective way of reducing plasma Lp(a). However, clinical benefits of lowering plasma Lp(a) have not been demonstrated, and specific therapeutic goals cannot be recommended at present. The structural similarity between apo(a) and plasminogen has generated several experimental observations indicating a prothombogenic and proatherogenic role of Lp(a), but the exact pathophysiological mechanisms have not been determined.

摘要

脂蛋白(a)[Lp(a)]是一类与低密度脂蛋白(LDL)相似的血浆脂蛋白,但含有一种与纤溶酶原具有显著同源性的独特载脂蛋白(a)。血浆Lp(a)作为一种数量遗传性状遗传,在白种人群中呈连续分布(<10~2000mg/L),其中高水平与动脉粥样硬化疾病风险增加相关。Lp(a)的生理作用尚不清楚,其代谢也不明确。血浆Lp(a)显然对饮食和药物治疗有抵抗性,而低密度脂蛋白清除术是目前降低血浆Lp(a)最有效的方法。然而,降低血浆Lp(a)的临床益处尚未得到证实,目前也无法推荐具体的治疗目标。载脂蛋白(a)与纤溶酶原之间的结构相似性产生了一些实验观察结果,表明Lp(a)具有促血栓形成和促动脉粥样硬化作用,但确切的病理生理机制尚未确定。

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