Bhakdi S
Institute of Medical Microbiology and Hygiene, Johannes Gutenberg University Mainz, Germany.
Clin Nephrol. 2003 Jul;60 Suppl 1:S49-52.
According to the textbooks, oxidative processes transform low density lipoprotein (LDL) to an atherogenic moiety. Oxidized LDL contains potentially harmful constituents that induce inflammatory responses in endothelial cells, smooth muscle cells and macrophages. The oxidation hypothesis, born 20 years ago through the work of Steinberg and colleagues [Steinberg et al. 1989], forms the basis for current discussions on the pathogenesis of atherosclerosis [Glass and Witztum 2000, Lusis 2000]. In the clinical setting, however, a puzzle relates to the failure of antioxidants to prevent and cure coronary heart disease; we here allude to just the most recent study [Brown et al. 2001]. More unobtrusively, experimental observations accumulating over the past years have laid the foundation for an alternative view on atherogenesis that will be outlined here.
根据教科书的说法，氧化过程会将低密度脂蛋白（LDL）转化为致动脉粥样硬化部分。氧化型LDL含有潜在有害成分，可在内皮细胞、平滑肌细胞和巨噬细胞中引发炎症反应。氧化假说于20年前由斯坦伯格及其同事的研究[斯坦伯格等人，1989年]提出，构成了当前关于动脉粥样硬化发病机制讨论的基础[格拉斯和维茨图姆，2000年；卢西斯，2000年]。然而，在临床环境中，一个谜题在于抗氧化剂未能预防和治愈冠心病；我们在此仅提及最近的一项研究[布朗等人，2001年]。更不引人注意的是，过去几年积累的实验观察结果为动脉粥样硬化发生的另一种观点奠定了基础，本文将对此进行概述。
