Srivastava D
Department of Pediatrics and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA.
Annu Rev Physiol. 2001;63:451-69. doi: 10.1146/annurev.physiol.63.1.451.
More children die from congenital heart defects (CHD) each year than are diagnosed with childhood cancer, yet the causes remain unknown. The remarkable conservation of genetic pathways regulating cardiac development in species ranging from flies to humans provides an opportunity to experimentally dissect the role of critical cardiogenic factors. Utilization of model biological systems has resulted in a molecular framework in which to consider the etiology of CHD. As whole genome sequencing and single nucleotide polymorphism data become available, identification of genetic mutations predisposing to CHD may allow preventive measures by modulation of secondary genetic or environmental factors. In this review, genetic pathways regulating cardiogenesis revealed by cross-species studies are reviewed and correlated with human CHD.
每年死于先天性心脏病(CHD)的儿童比被诊断患有儿童癌症的儿童更多,但其病因仍然不明。从果蝇到人类,调节心脏发育的遗传途径在物种间具有显著的保守性,这为通过实验剖析关键心脏发生因子的作用提供了机会。利用模式生物系统已形成了一个分子框架,用以思考CHD的病因。随着全基因组测序和单核苷酸多态性数据的可得,识别易患CHD的基因突变可能会通过调节次要遗传或环境因素来采取预防措施。在本综述中,将对跨物种研究揭示的调节心脏发生的遗传途径进行综述,并与人类CHD进行关联。