Role of 8-nitro-cGMP and its redox regulation in cardiovascular electrop hilic signaling

Role of 8-nitro-cGMP and its redox regulation in cardiovascular electrop hilic signaling
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8-硝基-cGMP 及其氧化还原调节在心血管亲电子信号传导中的作用

DOI:
10.1016/j.yjmcc.2014.02.003
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发表时间:
2014
期刊:
影响因子:
5
通讯作者:
Toyama T and Akaike T
Toyama T and Akaike T
中科院分区:
医学2区
文献类型:
--
作者:
Nishida M;Toyama T and Akaike T

文献摘要

相似文献

心血管系统的结构和形态变化(心血管重构)是心血管疾病的主要临床结果。许多证据表明,由于活性氧(ROS)和/或ROS衍生的亲电代谢产物(亲电体)的过量产生而导致的还原/氧化(氧化还原)稳态的变形是心血管重塑的主要原因。气体递质,如一氧化氮(NO)和内源性亲电物质,被认为是主要的生物活性物质,并已在生理和病理心血管事件的背景下进行了广泛的研究。我们最近发现,硫化氢相关的反应性物质作为有效的亲核试剂起作用,以消除由NO衍生的亲电副产物诱导的信号蛋白的亲电修饰(例如,8-硝基鸟苷3′,5 ′-环一磷酸和硝基油酸)。在这篇综述中,我们讨论了目前对亲电物质和亲核物质对心血管病理生理学的氧化还原控制的理解。我们认为,调节亲电介质介导的蛋白质半胱氨酸巯基的翻译后修饰可能是心血管疾病的一种新的治疗策略。这篇文章是题为“心血管系统中的氧化还原信号”的特刊的一部分。
Structural and morphological changes of the cardiovascular systems (cardiovascular remodeling) are a major clinical outcome of cardiovascular diseases. Many lines of evidences have implied that transfiguration of reduction/oxidation (redox) homeostasis due to excess production of reactive oxygen species (ROS) and/or ROS-derived electrophilic metabolites (electrophiles) is the main cause of cardiovascular remodeling. Gasotransmitters, such as nitric oxide (NO) and endogenous electrophiles, are considered major bioactive species and have been extensively studied in the context of physiological and pathological cardiovascular events. We have recently found that hydrogen sulfide-related reactive species function as potent nucleophiles to eliminate electrophilic modification of signaling proteins induced by NO-derived electrophilic byproducts (e.g., 8-nitroguanosine 3′,5′-cyclic monophosphate and nitro-oleic acid). In this review, we discuss the current understanding of redox control of cardiovascular pathophysiology by electrophiles and nucleophiles. We propose that modulation of electrophile-mediated post-translational modification of protein cysteine thiols may be a new therapeutic strategy of cardiovascular diseases. This article is part of a Special Issue entitled “Redox Signalling in the Cardiovascular System”.