TY - JOUR
T1 - Human congenital long QT syndrome
T2 - More than previously thought?
AU - Attali, Bernard
N1 - Funding Information:
This work is supported by the Israel Science Foundation (grant no. 540/01–1).
PY - 2002/6/1
Y1 - 2002/6/1
N2 - Mutations in KCNQ1 and KCNE1, the α- and β-subunits of the IKS K+ channel, produce the cardiac long QT (LQT) syndrome. These subunits are expressed in heart and inner ear, but also in epithelial tissues such as kidney or intestine where their functional roles have remained elusive. Recent work has shown that KCNE1-deficient mice display chronic hypokalemia and hyperaldosteronism. These results have significant implications for human congenital LQT syndromes because hypokalemia increases the risk of ventricular arrhythmia and cardiac sudden death.
AB - Mutations in KCNQ1 and KCNE1, the α- and β-subunits of the IKS K+ channel, produce the cardiac long QT (LQT) syndrome. These subunits are expressed in heart and inner ear, but also in epithelial tissues such as kidney or intestine where their functional roles have remained elusive. Recent work has shown that KCNE1-deficient mice display chronic hypokalemia and hyperaldosteronism. These results have significant implications for human congenital LQT syndromes because hypokalemia increases the risk of ventricular arrhythmia and cardiac sudden death.
UR - http://www.scopus.com/inward/record.url?scp=0036591655&partnerID=8YFLogxK
U2 - 10.1016/S0165-6147(02)02029-1
DO - 10.1016/S0165-6147(02)02029-1
M3 - סקירה
AN - SCOPUS:0036591655
VL - 23
SP - 249
EP - 251
JO - Trends in Pharmacological Sciences
JF - Trends in Pharmacological Sciences
SN - 0165-6147
IS - 6
ER -