Redox signaling in the cardiomyocyte: From physiology to failure
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- 作者：Celio X.C. Santos ; Sadaf Raza ; Ajay M. Shah ; ajay.shah@kcl.c.uk" class="auth_mail" title="E-mail the corresponding author
- 关键词：AKAP ; A-kinase anchoring protein ; CaMKII ; Ca2+/calmodulin-dependent kinase II ; ECC ; excitation contraction coupling ; elF2α ; eukaryotic initiation factor 2α ; ER ; endoplasmic reticulum ; ETC ; Electron transport chain ; GPCR ; G-protein coupled receptor ; Hif1 ; hypoxia-inducible factor 1 ; HDAC ; histone deacetylase ; MEF2 ; myocyte enhancer factor-2 ; Nox ; NADPH oxidase ; NO ; nitric oxide ; NOS ; nitric oxide synthase ; Nrf2 ; nuclear factor erythroid-derived 2-like 2 ; PHD ; prolyl hydroxylase ; PKA ; protein kina
- 刊名：International Journal of Biochemistry and Cell Biology
- 出版年：2016
- 出版时间：May 2016
- 年：2016
- 卷：74
- 期：Complete
- 页码：145-151
- 全文大小：1121 K
文摘
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The view that ROS are either harmful or beneficial is very simplistic.
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ROS can mediate specific post-translational modifications of biomolecules involved in intracellular signaling networks.
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Redox signaling involves spatially and temporally confined ROS production which modulates activity of signaling molecules.
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The NADPH oxidase proteins Nox2 and Nox4 are major enzymatic sources of ROS involved in cell signaling in cardiomyocytes.
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Redox signaling in the heart is involved in acute and chronic cardiac adaptations to diverse stresses.