Redox modification of cell signaling in the cardiovascular system

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• 作者：Dan Shao^a ; Shin-ichi Oka^a ; Christopher D. Brady^a ; Judith Haendeler^b ; Philip Eaton^c ; Junichi Sadoshima^a ; ^{sadoshju@umdnj.edu}
• 关键词：AngII ; angiotensin II ; ASK1 ; apoptosis signal-regulating kinase 1 ; BDNF ; brain-derived neurotrophic factor ; BH4 ; tetrahydrobiopterin ; CaMKII ; Ca2+/calmodulin-dependent protein kinase II ; cGMP ; cyclic guanosine monophosphate ; ETC ; electron transport chain
• 刊名：Journal of Molecular and Cellular Cardiology
• 出版年：2012
• 期刊代码：171_00222828
• 类别：bio
• 出版时间：March, 2012
• 卷：52
• 期：3
• 页码：550-558
• 文件大小：803 K

摘要

Oxidative stress is presumed to be involved in the pathogenesis of many diseases, including cardiovascular disease. However, oxidants are also generated in healthy cells, and increasing evidence suggests that they can act as signaling molecules. The intracellular reduction-oxidation (redox) status is tightly regulated by oxidant and antioxidant systems. Imbalance between them causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, leading to dysregulation. In this review, we will briefly summarize the aspects of ROS generation and neutralization mechanisms in the cardiovascular system. ROS can regulate cell signaling through oxidation and reduction of specific amino acids within proteins. Structural changes during post-translational modification allow modification of protein activity which can result in altered cellular function. We will focus on the molecular basis of redox protein modification and how this regulatory mechanism affects signal transduction in the cardiovascular system. Finally, we will discuss some techniques applied to monitoring redox status and identifying redox-sensitive proteins in the heart. This article is part of a Special Section entitled 鈥淧ost-translational Modification.鈥?/div>