Abstract：
:Cardiac hypertrophy is an adaptive process against increased work loads; however, hypertrophy also presents substrates for lethal ventricular arrhythmias, resulting in sudden arrhythmic deaths that account for about one third of deaths in cardiac hypertrophy. To maintain physiological cardiac function in the face of increased work loads, hypertrophied cardiomyocytes undergo K(+) channel remodeling that provides a prolongation in action potential duration and an increase in Ca(2+) entry. Increased Ca(2+) entry, in turn, activates signaling mechanisms including a calcineruin/NFAT pathway to permit remodeling of the K(+) channels. This results in a positive feedback loop between the K(+) channel remodeling and altered Ca(2+) handling; this loop may represent a potential therapeutic target against sudden arrhythmic deaths in cardiac hypertrophy. The purposes of this review are to: (1) discuss types of K(+) channels and their mRNA that undergo remodeling in cardiac hypertrophy; (2) report on recent research on molecular mechanisms of K(+) channel remodeling; and (3) address physiological events underlying new therapeutic modalities to ameliorate arrhythmias and sudden death in cardiac hypertrophy.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Furukawa T,Kurokawa Jdoi
10.1016/j.yjmcc.2006.07.021subject
Has Abstractpub_date
2006-11-01 00:00:00pages
753-61issue
5eissn
0022-2828issn
1095-8584pii
S0022-2828(06)00734-6journal_volume
41pub_type
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journal_title：Journal of molecular and cellular cardiology
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journal_title：Journal of molecular and cellular cardiology
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pub_type： 杂志文章
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journal_title：Journal of molecular and cellular cardiology
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pub_type： 杂志文章,评审
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pub_type： 杂志文章
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更新日期：1999-03-01 00:00:00
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pub_type： 杂志文章
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更新日期：2008-06-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/0022-2828(91)90190-w
更新日期：1991-12-01 00:00:00
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更新日期：2019-02-01 00:00:00
