Yip Agustin G, Ma Qianli, Wilcox Marsha, Panhuysen Carolien I, Farrell John, Farrer Lindsay A, Wyszynski Diego F
Genetics Program, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA.
BMC Genet. 2003 Dec 31;4 Suppl 1(Suppl 1):S100. doi: 10.1186/1471-2156-4-S1-S100.
Atherogenic dyslipidemia (AD) is a common feature in persons with premature coronary heart disease. While several linkage studies have been carried out to dissect the genetic etiology of lipid levels, few have investigated the AD lipid triad comprising elevated serum triglyceride, small low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) cholesterol levels. Here we report the results of a whole-genome screen for AD using the Framingham Heart Study population.
Our analyses provide some evidence for linkage to AD on chromosomes 1q31, 3q29, 10q26, 14p12, 14q13, 16q24, 18p11, and 19q13.
AD susceptibility is modulated by multiple genes in different chromosomes. Our study confirms results from other populations and suggests new areas of potential importance.
致动脉粥样硬化性血脂异常（AD）是早发性冠心病患者的常见特征。虽然已经开展了多项连锁研究来剖析血脂水平的遗传病因，但很少有研究调查由血清甘油三酯升高、小而密低密度脂蛋白（LDL）颗粒以及高密度脂蛋白（HDL）胆固醇水平降低组成的AD血脂三联征。在此，我们报告使用弗雷明汉心脏研究人群进行的AD全基因组筛查结果。
我们的分析为1号染色体长臂31区、3号染色体长臂29区、10号染色体长臂26区、14号染色体短臂12区、14号染色体长臂13区、16号染色体长臂24区、18号染色体短臂11区和19号染色体长臂13区与AD的连锁提供了一些证据。
AD易感性受不同染色体上多个基因的调控。我们的研究证实了其他人群的研究结果，并提示了潜在重要的新领域。
