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CYBA gene variants as biomarkers for coronary artery disease.

机译:CYBA基因变异作为冠状动脉疾病的生物标记。

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Oxidative stress plays a key role in the pathophysiology of coronary artery disease, and constitutes a common mechanism behind the risk factors associated with this disease such as atherosclerosis, hypertension, diabetes and the metabolic syndrome. Oxidative stress is defined as an imbalance between the production of reactive oxygen and nitrogen species and the detoxification by the appropriate cellular systems. Reactive oxygen species induce cardiovascular dysfunction by modulating cell contraction/dilation, migration, growth/apoptosis and extracellular matrix protein turnover, which contribute to vascular and cardiac remodeling. In the last decade, the NADPH oxidase family has emerged as one of the most relevant sources of reactive oxygen species within the cardiovascular system. Recent data suggest a significant role of the genetic background in NADPH oxidase regulation. Common genetic polymorphisms within the promoter and exonic sequences of CYBA, the gene that encodes the p22phox subunit of the NADPH oxidase, have been characterized in the context of cardiovascular diseases. This review aims to present the current state of research into these polymorphisms with regards to their relationship to coronary artery disease.
机译:氧化应激在冠状动脉疾病的病理生理中起着关键作用,并构成与该疾病相关的危险因素(如动脉粥样硬化,高血压,糖尿病和代谢综合征)的共同机制。氧化应激定义为活性氧和氮物质的产生与适当细胞系统解毒之间的不平衡。活性氧通过调节细胞的收缩/扩张,迁移,生长/凋亡和细胞外基质蛋白更新来诱发心血管功能障碍,这有助于血管和心脏的重塑。在过去的十年中,NADPH氧化酶家族已成为心血管系统中最重要的活性氧来源之一。最近的数据表明遗传背景在NADPH氧化酶调节中的重要作用。在心血管疾病的背景下,CYBA的启动子和外显子序列(编码NADPH氧化酶的p22phox亚基的基因)内的常见遗传多态性已得到表征。本文旨在就这些多态性与冠状动脉疾病的关系提出目前的研究状态。

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