Platt Frances M, Wassif Christopher, Colaco Alexandria, Dardis Andrea, Lloyd-Evans Emyr, Bembi Bruno, Porter Forbes D
Department of Pharmacology, University of Oxford, Oxford OX1 3QT, United Kingdom; email:
Annu Rev Genomics Hum Genet. 2014;15:173-94. doi: 10.1146/annurev-genom-091212-153412.
Cholesterol plays a key role in many cellular processes, and is generated by cells through de novo biosynthesis or acquired from exogenous sources through the uptake of low-density lipoproteins. Cholesterol biosynthesis is a complex, multienzyme-catalyzed pathway involving a series of sequentially acting enzymes. Inherited defects in genes encoding cholesterol biosynthetic enzymes or other regulators of cholesterol homeostasis result in severe metabolic diseases, many of which are rare in the general population and currently without effective therapy. Historically, these diseases have been viewed as discrete disorders, each with its own genetic cause and distinct pathogenic cascades that lead to its specific clinical features. However, studies have recently shown that three of these diseases have an unanticipated mechanistic convergence. This surprising finding is not only shedding light on details of cellular cholesterol homeostasis but also suggesting novel approaches to therapy.
胆固醇在许多细胞过程中发挥关键作用,细胞可通过从头生物合成产生胆固醇,也可通过摄取低密度脂蛋白从外源获取胆固醇。胆固醇生物合成是一条复杂的、由多酶催化的途径,涉及一系列依次作用的酶。编码胆固醇生物合成酶或其他胆固醇稳态调节因子的基因发生遗传性缺陷会导致严重的代谢疾病,其中许多在普通人群中较为罕见,目前尚无有效治疗方法。从历史上看,这些疾病被视为离散性疾病,每种疾病都有其自身的遗传病因和独特的致病级联反应,导致其特定的临床特征。然而,最近的研究表明,其中三种疾病存在意想不到的机制趋同现象。这一惊人发现不仅揭示了细胞胆固醇稳态的细节,还为治疗提供了新方法。