Department of Laboratory Medicine, Jikei University Kashiwa Hospital, Chiba, Japan.
Clin Chim Acta. 2010 Dec 14;411(23-24):1875-82. doi: 10.1016/j.cca.2010.08.038. Epub 2010 Sep 9.
Many lines of evidence suggest that oxidized low-density lipoprotein (LDL) is implicated in the pathogenesis of atherosclerotic vascular diseases. This review summarizes a diversity of mechanisms proposed for LDL oxidation serving for the so-called "LDL oxidation hypothesis of atherogenesis".
We investigated the literature and our research results related to mechanisms of LDL oxidation and its atherogenesis. LDL oxidation is catalyzed by transition metal ions and several free radicals, and LDL is also oxidized by some oxidizing enzymes. In this way, LDL can be converted to a form that is recognized specifically by and with high affinity to macrophage scavenger receptors, leading to foam cell formation, the defining characteristic of fatty streak lesions.
Several pathways are involved in the promotion of LDL oxidation in vitro and in vivo, but it would appear that the physiologically relevant mechanisms of LDL oxidation are still imperfectly understood. The underlying mechanisms of LDL oxidation must be further explored to reveal appropriate ways for the diagnosis and treatment of atherosclerosis and its relevant diseases.
大量证据表明,氧化型低密度脂蛋白(LDL)与动脉粥样硬化血管疾病的发病机制有关。本综述总结了多种 LDL 氧化的机制,这些机制被称为“动脉粥样硬化发病的 LDL 氧化假说”。
我们研究了与 LDL 氧化及其动脉粥样硬化发病机制相关的文献和我们的研究结果。LDL 氧化由过渡金属离子和几种自由基催化,LDL 也可被一些氧化酶氧化。这样,LDL 可转化为一种形式,这种形式可被巨噬细胞清道夫受体特异性识别并具有高亲和力,导致泡沫细胞形成,这是脂肪条纹病变的特征性表现。
体外和体内有几种途径可促进 LDL 氧化,但似乎生理相关的 LDL 氧化机制仍未被完全理解。LDL 氧化的潜在机制需要进一步探索,以揭示诊断和治疗动脉粥样硬化及其相关疾病的合适方法。