Genetics in childhood atherosclerosis

详细信息    查看全文

• 作者：Hegele ; Robert A.
• 关键词：Inflammation ; Immunity ; Lipoproteins ; Small effects ; Complex disease
• 刊名：Progress in Pediatric Cardiology
• 出版年：1998
• 出版时间：December 1, 1998
• 年：1998
• 卷：9
• 期：3
• 页码：213-224
• 全文大小：127 K

文摘

It is generally accepted that atherosclerosis is the extreme manifestation of what begins as a protective, fibroproliferative response to injury. Atherosclerosis can become pathological as a result of chronic, excessive exposure to particular causative agents. Several pathophysiological systems, including the inflammatory response, the immune response, cellular growth and proliferation, lipoprotein metabolism and coagulation, each of which operates as the result of the contributions of numerous gene products, can contribute to atherosclerosis either individually or in concert. In theory, identifying the genetic component(s) of atherosclerosis has become possible with molecular technologies and analytical methods. Reductionist experimental models have produced a list of several hundred candidate genes for the study of the genetic component of atherosclerosis. Within some families and isolated communities, the effect of a single gene upon atherosclerosis susceptibility may be profound, such as in the case of mutations within the gene encoding the low density lipoprotein receptor. However, at the level of the general population, particular candidate genes have small effects on atherosclerosis, or on one of its intermediate phenotypes. Furthermore, there are other factors, such as pleiotropy, epistasis, variations in genetic background, differences in individual environmental landscape, non-linear interactions among gene products and interactions between genes and the environment, which can confound the study of the genetic component of atherosclerosis.