Adenosine triphosphate-sensitive potassium channels and cardiomyopathies (Review)

被引:6
|
作者
Liu, Zhongwei [1 ]
Cai, Hui [2 ]
Dang, Yonghui [3 ]
Qiu, Chuan [4 ]
Wang, Junkui [1 ]
机构
[1] Shaanxi Prov Peoples Hosp, Dept Cardiol, 256 Youyi West Rd, Xian 710068, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Dept Anesthesiol, Affiliated Hosp 1, Xian 710061, Shaanxi, Peoples R China
[3] Xi An Jiao Tong Univ, Sch Med, Coll Med & Forens, Xian 710061, Shaanxi, Peoples R China
[4] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Biostat & Bioinformat, New Orleans, LA 70112 USA
基金
中国国家自然科学基金;
关键词
cardiomyopathy; K-ATP channels; K-ATP CHANNELS; SULFONYLUREA RECEPTOR; DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; VENTRICULAR-FIBRILLATION; EARLY REPOLARIZATION; CARDIAC-HYPERTROPHY; KESHAN-DISEASE; HEART-FAILURE; BINDING-SITE;
D O I
10.3892/mmr.2015.4714
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cardiomyopathies have been indicated to be one of the leading causes of heart failure. Though it was indicated that genetic defects, viral infection and trace element deficiency were among the causes of cardiomyopathy, the etiology has remained to be fully elucidated. Cardiomyocytes require large amounts of energy to maintain their normal biological functions. Adenosine triphosphate-sensitive potassium channels (K-ATP), composed of inward-rectifier potassium ion channel and sulfonylurea receptor subunits, are present on the cell surface and mitochondrial membrane of cardiac muscle cells. As metabolic sensors sensitive to changes in intracellular energy levels, K-ATP adapt electrical activities to metabolic challenges, maintaining normal biological functions of myocytes. It is implied that malfunctions, mutations and altered expression of K-ATP are associated with the pathogenesis of conditions including c hypertrophy, diabetes as well as dilated, ischemic and endemic cardiomyopathy. However, the current knowledge is only the tip of the iceberg and the roles of K-ATP in cardiomyopathies largely remain to be elucidated in future studies.
引用
收藏
页码:1447 / 1454
页数:8
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