Genetic Predispositions to Heart Failure

被引：0
作者：
Koh W. [1 ]
Wong C. [2 ]
Tang W.H.W. [3 ]
机构：
[1] Department of Pediatric Cardiology, Pediatrics Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, 44195, OH
[2] Center for Clinical Genomics, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, 44195, OH
[3] Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, Desk J3-4, Cleveland, 44195, OH
来源：
Current Cardiovascular Risk Reports | 2016年 / 10卷 / 12期
基金：
美国国家卫生研究院;
关键词：
Cardiomyopathy; Channelopathy; Familial; Genetics; Genome-Wide Association Studies (GWAS); Heart failure;
D O I：
10.1007/s12170-016-0525-2
中图分类号：
学科分类号：
摘要：
Heart failure can be caused by either acquired or inherited cardiovascular diseases. With the rising incidence of heart failure (HF), there is a need to further understand the molecular pathogenesis of HF. There has been growing interest in the role of genetic predisposition for developing HF, not only in inherited cardiomyopathies but also in acquired cardiovascular diseases. There have been expanding knowledge bases in specific pathogenic variants of sarcomeric genes, as well as genes encoding structural and cytoskeleton proteins, ion channels, calcium cycling proteins, nuclear proteins or transcriptomic factors, and even mitochondrial genes. Beyond inherited cardiomyopathies, several genome-wide association studies have identified novel genes associated with HF, yet the pathophysiologic contributions and their propensities of therapeutic targeting remains unresolved. © 2016, Springer Science+Business Media New York.
引用
收藏
相关论文
共 78 条
[31]  
Stark K., Esslinger U.B., Reinhard W., Et al., Genetic association study identifies HSPB7 as a risk gene for idiopathic dilated cardiomyopathy, PLoS Genet, 6, 10, (2010)
[32]  
van den Boogaard M., Barnett P., Christoffels V.M., From GWAS to function: genetic variation in sodium channel gene enhancer influences electrical patterning, Trends Cardiovasc Med, 24, 3, pp. 99-104, (2014)
[33]  
Vasan R.S., Glazer N.L., Felix J.F., Et al., Genetic variants associated with cardiac structure and function: a meta-analysis and replication of genome-wide association data, JAMA, 302, 2, pp. 168-178, (2009)
[34]  
Villard E., Perret C., Gary F., Et al., A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy, Eur Heart J, 32, 9, pp. 1065-1076, (2011)
[35]  
Dorn G.W., The genomic architecture of sporadic heart failure, Circ Res, 108, 10, pp. 1270-1283, (2011)
[36]  
Ommen S.R., Hypertrophic cardiomyopathy, Curr Probl Cardiol, 36, 11, pp. 409-453, (2011)
[37]  
Kim L., Devereux R.B., Basson C.T., Impact of genetic insights into mendelian disease on cardiovascular clinical practice, Circulation, 123, 5, pp. 544-550, (2011)
[38]  
Towbin J.A., Bowles N.E., The failing heart, Nature, 415, 6868, pp. 227-233, (2002)
[39]  
Cahill T.J., Ashrafian H., Watkins H., Genetic cardiomyopathies causing heart failure, Circ Res, 113, 6, pp. 660-675, (2013)
[40]  
Morita H., Seidman J., Seidman C.E., Genetic causes of human heart failure, J Clin Invest, 115, 3, pp. 518-526, (2005)
12345678