期刊
COMPREHENSIVE PHYSIOLOGY
卷 3, 期 2, 页码 667-692出版社
WILEY
DOI: 10.1002/cphy.c110014
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类别
资金
- National Institutes of Health [HL63914, HL106256, HL113598]
- National Center of Research Resources (NCRR) [P20RR15581]
- American Heart Association [11GRNT7610161]
- American Diabetes Association Innovation Award [07-8-IN-08]
Forward genetic studies have identified several chloride (Cl-) channel genes, including CFTR, ClC-2, ClC-3, CLCA, Bestrophin, and Ano1, in the heart. Recent reverse genetic studies using gene targeting and transgenic techniques to delineate the functional role of cardiac Cl- channels have shown that Cl- channels may contribute to cardiac arrhythmogenesis, myocardial hypertrophy and heart failure, and cardioprotection against ischemia reperfusion. The study of physiological or pathophysiological phenotypes of cardiac Cl-channels, however, is complicated by the compensatory changes in the animals in response to the targeted genetic manipulation. Alternatively, tissue-specific conditional or inducible knockout or knockin animal models may be more valuable in the phenotypic studies of specific Cl- channels by limiting the effect of compensation on the phenotype. The integrated function of Cl- channels may involve multiprotein complexes of the Cl- channel subproteome. Similar phenotypes can be attained from alternative protein pathways within cellular networks, which are influenced by genetic and environmental factors. The phenomics approach, which characterizes phenotypes as a whole phenome and systematically studies the molecular changes that give rise to particular phenotypes achieved by modifying the genotype under the scope of genome/proteome/phenome, may provide more complete understanding of the integrated function of each cardiac Cl- channel in the context of health and disease. (C) 2013 American Physiological Society.
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