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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Redox-inflammatory synergy in the metabolic syndrome
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Redox-inflammatory synergy in the metabolic syndrome

机译:代谢综合征中的氧化还原-炎症协同作用

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摘要

Metabolic syndrome (MetS) comprises interrelated disease states including obesity, insulin resistance and type 2 diabetes (T2DM), dyslipidemia, and hypertension. Essential to normal physiological function, and yet massively damaging in excess, oxidative stress and inflammation are pivotal common threads among the pathologies of MetS. Increasing evidence indicates that redox and inflammatory dysregulation parallels the syndrome's physiological, biochemical, and anthropometric features, leading many to consider the pro-oxidative, pro-inflammatory milieu an unofficial criterion in itself. Left unchecked, cross-promotion of oxidative stress and inflammation creates a feed-forward cycle that can initiate and advance disease progression. Such redox-inflammatory integration is evident in the pathogenesis of obesity, insulin resistance and T2DM, atherogenic dyslipidemia, and hypertension, and is thus hypothesized to be the "common soil" from which they develop. The present review highlights the synergistic contributions of redox-inflammatory processes to each of the components of the MetS.
机译:代谢综合征(MetS)包括相互关联的疾病状态,包括肥胖,胰岛素抵抗和2型糖尿病(T2DM),血脂异常和高血压。 MetS病理学中至关重要的共同线索是,正常生理功能必不可少,但仍会造成巨大的过度破坏,氧化应激和炎症。越来越多的证据表明,氧化还原和炎性调节异常与该综合征的生理,生化和人体测量学特征相似,导致许多人将促氧化,促炎环境本身视为非官方标准。如果任其发展,氧化应激和炎症的交叉促进会产生一个前馈周期,该周期可以引发并促进疾病的发展。在肥胖,胰岛素抵抗和T2DM,动脉粥样硬化血脂异常和高血压的发病机理中,这种氧化还原-炎症整合是明显的,因此被认为是它们发展的“普通土壤”。本综述强调了氧化还原-炎症过程对MetS各个组成部分的协同作用。

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