Redox regulation of cardiac calcium channels and transporters

被引:463
作者
Zima, Aleksey V. [1 ]
Blatter, Lothar A. [1 ]
机构
[1] Loyola Univ, Stritch Sch Med, Dept Physiol, Maywood, IL 60153 USA
基金
美国国家卫生研究院;
关键词
Ca-channel; Ca-pump; e-c coupling; oxygen radicals; redox signaling;
D O I
10.1016/j.cardiores.2006.02.019
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Intracellular concentrations of redox-active molecules can significantly increase in the heart as a result of activation of specific signal transduction pathways or the development of certain pathophysiological conditions. Changes in the intracellular redox environment can affect many cellular processes, including the gating properties of ion channels and the activity of ion transporters. Because cardiac contraction is highly dependent on intracellular Ca2+ levels ([Ca2+](i)) and [Ca2+](i) regulation, redox modification of Ca2+ channels and transporters has a profound effect on cardiac function. The sarcoplasmic reticulum (SR) Ca2+ release channel, or ryanodine receptor (RyR), is one of the well-characterized redox-sensitive ion channels in the heart. The redox modulation of RyR activity is mediated by the redox modification of sulfhydryl groups of cysteine residues. Other key components of cardiac excitation-contraction (e-c) coupling such as the SR Ca2+ ATPase and L-type Ca2+ channel are subject to redox modulation. Redox-mediated alteration of the activity of ion channels and pumps is directly involved in cardiac pathologies such as ischemia-reperfusion injury. Significant bursts of reactive oxygen species (ROS) generation occur during reperfusion of the ischemic heart, and changes in the activity of the major components of [Ca2+](i) regulation, such as RyR, Na+-Ca2+ exchange and Ca2+ ATPases, are likely to play an important role in ischemia-related Ca2+ overload. This article summarizes recent findings on redox regulation of cardiac Ca2+ transport systems and discusses contributions of this redox regulation to normal and pathological cardiac function. (c) 2006 European Society of Cardiology. Published by Elsevier B.V All rights reserved.
引用
收藏
页码:310 / 321
页数:12
相关论文
共 119 条
  • [1] CRITICAL SULFHYDRYLS REGULATE CALCIUM RELEASE FROM SARCOPLASMIC-RETICULUM
    ABRAMSON, JJ
    SALAMA, G
    [J]. JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 1989, 21 (02) : 283 - 294
  • [2] S-glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide
    Adachi, T
    Weisbrod, RM
    Pimentel, DR
    Ying, J
    Sharov, VS
    Schöneich, C
    Cohen, RA
    [J]. NATURE MEDICINE, 2004, 10 (11) : 1200 - 1207
  • [3] Effects of hydroxyl radical and sulfhydryl reagents on the open probability of the purified cardiac ryanodine receptor channel incorporated into planar lipid bilayers
    Anzai, K
    Ogawa, K
    Kuniyasu, A
    Ozawa, T
    Yamamoto, H
    Nakayama, H
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 249 (03) : 938 - 942
  • [4] The skeletal muscle Ca2+ release channel has an oxidoreductase-like domain
    Baker, ML
    Serysheva, II
    Sencer, S
    Wu, YL
    Ludtke, SJ
    Jiang, W
    Hamilton, SL
    Chiu, W
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (19) : 12155 - 12160
  • [5] Nitric oxide synthases and cardiac muscle - Autocrine and paracrine influences
    Balligand, JL
    Cannon, PJ
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) : 1846 - 1858
  • [6] Calmodulin binding and inhibition of cardiac muscle calcium release channel (ryanodine receptor)
    Balshaw, DM
    Xu, L
    Yamaguchi, N
    Pasek, DA
    Meissner, G
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (23) : 20144 - 20153
  • [7] Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms
    Barouch, LA
    Harrison, RW
    Skaf, MW
    Rosas, GO
    Cappola, TP
    Kobeissi, ZA
    Hobai, IA
    Lemmon, CA
    Burnett, AL
    O'Rourke, B
    Rodriguez, ER
    Huang, PL
    Lima, JAC
    Berkowitz, DE
    Hare, JM
    [J]. NATURE, 2002, 416 (6878) : 337 - 340
  • [8] Antioxidant pyruvate inhibits cardiac formation of reactive oxygen species through changes in redox state
    Bassenge, E
    Sommer, O
    Schwemmer, M
    Bünger, R
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 279 (05): : H2431 - H2438
  • [9] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING
    BERRIDGE, MJ
    [J]. NATURE, 1993, 361 (6410) : 315 - 325
  • [10] Bers D.M., 2001, Excitation-Contraction Coupling and Cardiac Contractile Force, V2th