心脏发育过程中的信号调控机制研究
常 在, 杨中州*
(南京大学模式动物研究所,南京210061)

摘 要:摘 要:我国是出生缺陷高发国家,其中先天性心脏病在各类出生缺陷中居于首位,严重地影响我国的人口素质[1]。同样,后天性心脏血管疾病(心血管疾病)也是影响国民健康和社会发展的主要疾病[2]。近年来研究表明,所谓“后天性”心脏血管疾病虽然大多不在胚胎期表现出功能异常,但遗传因素在发病过程中也起关键作用,因此,“后天性”心血管疾病也有其发育生物学基础。在一些心血管疾病中,胚胎发育基因如ANF和b-MHC 的表达说明胚胎发育的某些机制参与了发病过程。由于出生缺陷和心血管疾病的防治是我国公共卫生和社会发展中亟待解决的重大健康问题,了解心血管系统正常发生发育规律和机制及发病机理并在此基础上建立新的防治策略和防治措施是生命科学需要解决的重大基础科学问题[1-2]。本文主要综述了目前模式动物,特别是小鼠心脏发育过程中的信号传导调控机制的研究现状及进展。
关键词:心脏;心血管疾病;先天性心脏病;胚胎发育;模式动物
中图分类号:R541; Q132.4; Q954.4  文献标识码:A

Mechanistic study of signal transduction in heart development
CHANG Zai, YANG Zhongzhou*
(Model Animal Research Center of Nanjing University, Nanjing 210061, China)

Abstract: Abstract: In China, the population quality is deteriorating by high rate of birth defects, among which congenital heart diseases are the most common. Similarly, postnatal cardiovascular disorders are becoming the main impediment to population health and social development. Recent studies have demonstrated that developmental biology is involved in the pathogenesis of postnatal cardiovascular disorders in that hereditary factors contribute to the progress of these diseases, although they fail to cause embryonic abnormalities. The fact that in some postnatal cardiovascular diseases, essential genes for embryogenesis such as ANF and beta-MHC are activated indicates that certain embryonic developmental mechanisms are engaged in the pathogenesis. Because the prevention of birth defects and cardiovascular disorders is one of the major issues that demands urgent solution for public health and social development, the understanding of normal developmental mechanisms and knowledge as well as pathogenesis of cardiovascular system is becoming increasingly important for the purpose to help establish novel and efficient strategy and measures of prevention. Here we briefly summarize the current research proceedings of signal transduction regulation in heart development of commonly used model animals with emphasis on mouse.
Key words: heart; cardiovascular diseases; congenital heart diseases; embryogenesis; model animals

Back to top