Lusis A J
Department of Medicine, Biology Institute, University of California, Los Angeles 90095, USA.
Nature. 2000 Sep 14;407(6801):233-41. doi: 10.1038/35025203.
Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.
动脉粥样硬化是一种发生于大动脉的疾病，是心脏病和中风的主要病因。在西方化社会中，它是约50%的所有死亡的潜在原因。流行病学研究已经揭示了与动脉粥样硬化相关的几个重要环境和遗传风险因素。然而，由于该疾病病因的复杂性，在确定所涉及的细胞和分子相互作用方面的进展受到了阻碍。在过去十年中，包括疾病的转基因小鼠模型在内的新研究工具的出现，使人们对将胆固醇代谢改变和其他风险因素与动脉粥样硬化斑块形成联系起来的分子机制有了更清晰的认识。现在很清楚，动脉粥样硬化不仅仅是衰老不可避免的退行性后果，而是一种慢性炎症状态，可因斑块破裂和血栓形成而转化为急性临床事件。
