The L-type Ca2+ Channel as a Potential Mediator of Pathology During Alterations in Cellular Redox State

被引：33
作者：
Hool, Livia C. [1 ,2 ]
机构：
[1] Univ Western Australia, Sch Biomed Biomol & Chem Sci, Crawley, WA, Australia
[2] Univ Western Australia, Western Australian Inst Med Res, Crawley, WA, Australia
来源：
HEART LUNG AND CIRCULATION | 2009年 / 18卷 / 01期
基金：
英国医学研究理事会;
关键词：
L-type calcium channel; Reactive oxygen species; Calcium; Hypoxia; Arrhythmia; Hypertrophy; ADRENERGIC-RECEPTOR STIMULATION; INDUCED CARDIAC-HYPERTROPHY; VENTRICULAR MYOCYTES; EARLY AFTERDEPOLARIZATIONS; NADPH OXIDASE; CALCIUM-CHANNELS; HYDROGEN-PEROXIDE; ALPHA(1C) SUBUNIT; ANGIOTENSIN-II; SUPEROXIDE-PRODUCTION;
D O I：
10.1016/j.hlc.2008.11.004
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
The L-type Ca2+ channel is the main route for calcium influx into cardiac myocytes and an important determinant of calcium homeostasis. There is now considerable evidence that the function of the L-type Ca2+ channel is influenced by the cell's redox state. Reactive oxygen species such as hydrogen peroxide and superoxide can regulate biological function by directly altering the thiol redox state of proteins. Under conditions where cellular redox state varies, L-type Ca2+ channel function and diastolic calcium levels can be significantly altered. This article will present the evidence for alterations in L-type Ca2+ channel function by reactive oxygen species and the potential role for the channel in development of acute electrophysiological instability or chronic pathological remodelling under conditions of persistent oxidative stress.
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页码：3 / 10
页数：8
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