Reductive potential - a savior turns stressor in protein aggregation cardiomyopathy.
Reductive potential - a savior turns stressor in protein aggregation cardiomyopathy.
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DOI：
10.1016/j.bbadis.2014.11.010
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发表时间：
2015-01
影响因子：
6.2
通讯作者：
Rajasekaran, Namakkal S.
中科院分区：
文献类型：
--
作者：
Narasimhan, Madhusudhanan;Rajasekaran, Namakkal S.
氧化还原稳态对于多种生理过程的基础信号传导至关重要，但向“氧化”或“还原”特性的单方面转变将改变细胞内氧化还原环境。通常，此类事件会影响细胞或细胞器的结构和天然功能。过去 6 年来的大量实验研究和临床试验表明，增强的氧自由基是引发多种人类疾病损害的主要刺激因素，包括心血管并发症，这支持了氧化应激 (OS) 理论。然而，在我们做出重大发现之前，“还原性应激 (RS)”与心脏健康之间的动态相互关系一直被大量的 OS 研究所掩盖（Rajasekaran 等人，2007 年）。值得注意的是，这一开创性的发现激发了人们对其他机制见解研究的极大兴趣，到目前为止，结果表明 RS 的作用与 OS 相似或更强。此外，根据我们自己的研究结果，我们坚信，能够持续产生还原型谷胱甘肽 (GSH)、还原型烟酰胺腺嘌呤二核苷酸磷酸 (NADPH) 的途径的组成性激活将导致 RS 并损害通过无害的促氧化事件运行的基础细胞信号传导机制，进而破坏控制健康细胞生理学的单个和/或关键细胞过程的组合，例如生长、成熟、分化、存活、死亡等。在这里，我们讨论了 RS 作为人类主要心脏病相关病理生理学的因果或促成因素的作用。
Redox homeostasis is essential for basal signaling of several physiological processes, but a unilateral shift towards an ‘oxidative’ or ‘reductive’ trait will alter intracellular redox milieu. Typically, such an event influences the structure and the native function of a cell or an organelle. Numerous experimental research and clinical trials over the last 6 decades have demonstrated that enhanced oxygen-derived free radicals constitutes a major stimuli to trigger damage in several human diseases, including cardiovascular complications supporting the theory of oxidative stress (OS). However, until our key discovery, the dynamic interrelationship between “Reductive Stress (RS)” and cardiac health has been obscured by overwhelming OS studies (Rajasekaran et al., 2007). Notably, this seminal finding spurred considerable interest in investigations of other mechanistic insights, and thus far the results indicate a similar or stronger role for RS, than that of OS. In addition, from our own findings we strongly believe that constitutive activation of pathways that enable sustained generation of reducing equivalents glutathione (GSH), reduced nicotinamide adenine dinucleotide phosphate (NADPH) will cause RS and impair the basal cellular signaling mechanisms operating through harmless pro-oxidative events, in turn, disrupting single and/or a combination of key cellular processes such as growth, maturation, differentiation, survival, death etc., that govern healthy cell physiology. Here, we have discussed the role of RS as a causal or contributing factor in relevant pathophysiology of a major cardiac disease of human origin.
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影响因子：
56.9
作者：
HWANG, C;SINSKEY, AJ;LODISH, HF
通讯作者：
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影响因子：
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通讯作者：
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