期刊
CURRENT OPINION IN PHARMACOLOGY
卷 15, 期 -, 页码 68-73出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2013.12.003
关键词
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资金
- Alexander von Humboldt-Foundation (Feodor Lynen Fellowship)
- National Institutes of Health [R01 NS08174]
- Deutsche Forschungsgemeinschaft [Po137/41-1]
- Hertie-Foundation [P2040097]
The non-selective Transient Receptor Potential Melastatin 4 (TRPM4) cation channel is abundantly expressed in cardiac cells, being involved in several aspects of cardiac rhythmicity, including cardiac conduction, pace making and action-potential repolarization. Dominantly inherited mutations in the TRPM4 gene are associated with the cardiac bundle-branch disorder progressive familial heart block type I (PFHBI) and isolated cardiac conduction disease (ICCD) giving rise to atrio-ventricular conduction block (AVB), right bundle branch block, bradycardia, and the Brugada syndrome. The mutant phenotypes closely resemble those associated with mutations in the SCN5A gene, encoding the voltage-gated Na+ channel Na(v)1.5. These observations and the unexpected partnership with sulfonylurea-receptors (SURs) makes the TRPM4 channel a promising novel target for treatment of cardiac disorders.
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