IK1 and cardiac hypoxia: After the long and short QT syndromes, what else can go wrong with the inward rectifier K+ currents?

Journal of Molecular and Cellular Cardiology

Volumn 43, Issue 1, 2007, Pages 15-17

  Xu, Yanfang ^a,c   Zhang, Qian ^a   Chiamvimonvat, Nipavan ^a,b  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b VETERANS AFFAIRS MEDICAL CENTER   (United States)

^c HEBEI MEDICAL UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATASE (POTASSIUM); INWARDLY RECTIFYING POTASSIUM CHANNEL;

ARRHYTHMOGENESIS; DOWN REGULATION; EDITORIAL; HEART ATRIUM FIBRILLATION; HEART FAILURE; HEART MUSCLE ISCHEMIA; HUMAN; LONG QT SYNDROME; PRIORITY JOURNAL; SHORT QT SYNDROME; UPREGULATION; CELL HYPOXIA; CLASSIFICATION; GENETICS; METABOLISM; MUTATION; NOTE;

ATRIAL FIBRILLATION; CELL HYPOXIA; DOWN-REGULATION; HEART FAILURE; HUMANS; LONG QT SYNDROME; MUTATION; POTASSIUM CHANNELS, INWARDLY RECTIFYING;

EID: 34250166524     PISSN: 00222828     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2007.04.015     Document Type: Editorial

References (33)

1. Hutter O.F., and Noble D. Rectifying properties of heart muscle. Nature 188 (1960) 495
2. + current during the action potential of guinea pig ventricular myocytes. Biophys. J. 60 (1991) 1534-1539
3. Nichols C.G., and Lopatin A.N. Inward rectifier potassium channels. Annu. Rev. Physiol. 59 (1997) 171-191
4. +-mediated vasodilation. Circ. Res. 87 (2000) 160-166
5. K1) in rabbit cardiomyocytes: evidence for heteromeric co-assembly of Kir2.1 and Kir2.2. J. Physiol. 550 (2003) 365-372
6. Plaster N.M., Tawil R., Tristani-Firouzi M., Canun S., Bendahhou S., Tsunoda A., et al. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome. Cell 105 (2001) 511-519
7. Miake J., Marban E., and Nuss H.B. Functional role of inward rectifier current in heart probed by Kir2.1 overexpression and dominant-negative suppression. J. Clin. Invest. 111 (2003) 1529-1536
8. K1 in the mouse heart leads to altered cardiac excitability. J. Mol. Cell. Cardiol. 35 (2003) 367-378
9. Priori S.G., Pandit S.V., Rivolta I., Berenfeld O., Ronchetti E., Dhamoon A., et al. A novel form of short QT syndrome (SQT3) is caused by a mutation in the KCNJ2 gene. Circ. Res. 96 (2005) 800-807
10. Xia M., Jin Q., Bendahhou S., He Y., Larroque M.M., Chen Y., et al. A Kir2.1 gain-of-function mutation underlies familial atrial fibrillation. Biochem. Biophys. Res. Commun. 332 (2005) 1012-1019
11. K1 in the mouse heart leads to multiple abnormalities of cardiac excitability. Am. J. Physiol.: Heart Circ. Physiol. 287 (2004) H2790-H2802
12. K1) in the mouse heart accelerates and stabilizes rotors. J. Physiol. 578 (2007) 315-326
13. Keating M.T., and Sanguinetti M.C. Molecular and cellular mechanisms of cardiac arrhythmias. Cell 104 (2001) 569-580
14. Kannankeril P.J., and Roden D.M. Drug-induced long QT and torsade de pointes: recent advances. Curr. Opin. Cardiol. 22 (2007) 39-43
15. K1 underlies early action potential shortening during hypoxia in the mouse heart. J. Mol. Cell. Cardiol. (2007)
16. Lopes C.M., Zhang H., Rohacs T., Jin T., Yang J., and Logothetis D.E. Alterations in conserved Kir channel-PIP2 interactions underlie channelopathies. Neuron 34 (2002) 933-944
17. Ballester L.Y., Benson D.W., Wong B., Law I.H., Mathews K.D., Vanoye C.G., et al. Trafficking-competent and trafficking-defective KCNJ2 mutations in Andersen syndrome. Hum. Mutat. 27 (2006) 388
18. Nagase S., Kusano K.F., Yoshida M., and Ohe T. Electrophysiologic characteristics of an Andersen syndrome patient with KCNJ2 mutation. Heart Rhythm 4 (2007) 512-515
19. K1: a simulation study. Am. J. Physiol.: Heart Circ. Physiol. 291 (2006) H2597-H2605
20. K1 mutations in human left ventricular myocytes and tissue. Am. J. Physiol.: Heart Circ. Physiol. 292 (2007) H549-H559
21. Tsuboi M., and Antzelevitch C. Cellular basis for electrocardiographic and arrhythmic manifestations of Andersen-Tawil syndrome (LQT7). Heart Rhythm 3 (2006) 328-335
22. Nattel S. Remodeling of cardiac inward-rectifier currents: an often-overlooked contributor to arrhythmogenic states. J. Mol. Cell. Cardiol. 35 (2003) 1395-1398
23. K1 in rat ventricular cells: a novel paradigm for arrhythmia in heart failure?. Cardiovasc. Res. 68 (2005) 204-212
24. Brugada R., Hong K., Dumaine R., Cordeiro J., Gaita F., Borggrefe M., et al. Sudden death associated with short-QT syndrome linked to mutations in HERG. Circulation 109 (2004) 30-35
25. Bellocq C., van Ginneken A.C., Bezzina C.R., Alders M., Escande D., Mannens M.M., et al. Mutation in the KCNQ1 gene leading to the short QT-interval syndrome. Circulation 109 (2004) 2394-2397
26. K1 in action potential shortening associated with atrial fibrillation in humans. Cardiovasc. Res. 66 (2005) 493-502
27. + channels. Diabetes 53 Suppl. 3 (2004) S104-S112
28. Miki T., and Seino S. Roles of KATP channels as metabolic sensors in acute metabolic changes. J. Mol. Cell. Cardiol. 38 (2005) 917-925
29. ATP channels in health and disease. J. Mol. Cell. Cardiol. 38 (2005) 937-943
30. K1 in the myocardial response to hypoxia. Cardiovasc. Res. 25 (1991) 17-26
31. + conductance during metabolic inhibition by cyanide in guinea pig ventricular myocytes. Nippon Ika Daigaku Zasshi 57 (1990) 308-321
32. Lopatin A.N., Makhina E.N., and Nichols C.G. Potassium channel block by cytoplasmic polyamines as the mechanism of intrinsic rectification. Nature 372 (1994) 366-369
33. Ruiz Petrich E., Ponce Zumino A., and Schanne O.F. Early action potential shortening in hypoxic hearts: role of chloride current(s) mediated by catecholamine release. J. Mol. Cell. Cardiol. 28 (1996) 279-290