https://scholars.lib.ntu.edu.tw/handle/123456789/536724
標題: | Molecular genetic studies in atrial fibrillation | 作者: | LING-PING LAI JIUNN-LEE LIN Huang S.K.S. |
關鍵字: | Atrial fibrillation; Genetics; Linkage analysis; Potassium channel | 公開日期: | 2003 | 卷: | 100 | 期: | 3 | 起(迄)頁: | 109-113 | 來源出版物: | Cardiology | 摘要: | Atrial fibrillation is a complex disease. Its etiologies are diverse and genetic factors may also contribute to this disease. With the advent of modern molecular biology technology, it is now possible to explore the genetic components in the pathogenesis of atrial fibrillation. Past molecular genetic studies on atrial fibrillation in the literature can be divided into linkage analysis studies and association studies. The subjects for linkage analysis studies are pedigrees of probands with Mendelian hereditary atrial fibrillation. The first locus identified for autosomal dominant atrial fibrillation locates at 10q22-q24. However, the exact gene is still unknown. Another linkage analysis study in Chinese revealed that LQT1 gene (IKs α-subunit) was the responsible gene. A missense mutation in the I Ks α-subunit results in a gain of function, which is important in causing atrial fibrillation. The third known locus for familial atrial fibrillation locates at 6q14-16. The responsible gene remains still unknown. The other type of studies takes the case-control design (association studies) and the subjects have multigenic atrial fibrillation. In a study in a Japanese population, it was reported that the angiotensin-converting enzyme insertion/deletion polymorphism was not associated with atrial fibrillation. On the other hand, researchers in Taiwan reported that a nonsynonymous single nucleotide polymorphism of the LQT5 gene (IKs β-subunit) is associated with atrial fibrillation. In summary, there is growing evidence showing that genetic factors are important in the pathogenesis of atrial fibrillation. We expect that more genes responsible for or contributing to atrial fibrillation will be identified in the future and these will elucidate the molecular mechanisms of atrial fibrillation. Copyright ? 2003 S. Karger AG, Basel. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0345257747&doi=10.1159%2f000073910&partnerID=40&md5=66ff6a90164ed63fa2831ae57fe1822c https://scholars.lib.ntu.edu.tw/handle/123456789/536724 |
ISSN: | 0008-6312 | DOI: | 10.1159/000073910 | SDG/關鍵字: | ion channel; animal; animal model; comparative study; disease association; dominant gene; female; gene identification; gene location; gene locus; genetic analysis; genetic linkage; genetic polymorphism; genetic predisposition; genetics; heart atrium fibrillation; human; Japan; male; methodology; missense mutation; molecular biology; molecular genetics; mouse; pathogenesis; pathophysiology; priority journal; review; sensitivity and specificity; transgenic mouse; Animals; Atrial Fibrillation; Female; Genes, Dominant; Genetic Predisposition to Disease; Humans; Ion Channels; Linkage (Genetics); Male; Mice; Mice, Transgenic; Models, Animal; Molecular Biology; Sensitivity and Specificity |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。