摘要
血管内皮是血管的最内层,维持血管收缩和血管舒张。血管张力的丧失是心血管疾病的标志。许多因素,如肾素-血管紧张素-醛固酮系统、激酶、生长因子等的过度激活,在血管磨损的诱导和进展中起着至关重要的作用。有趣的是,这些途径的失调要么增强氧化应激的强度,要么这些途径受到氧化应激的影响。因此,氧化应激被认为是血管内皮功能障碍进展的关键罪魁祸首。由活性氧和氮物质诱导的氧化应激导致基因表达异常、信号转导改变和通路激活,导致血管损伤的诱导和进展。此外,已经注意到许多抗氧化剂在预防血管内皮功能障碍的发展方面具有有希望的治疗潜力。因此,我们专注于氧化应激信号传导的当前观点,以评估氧化应激在血管内皮功能障碍进展中起关键作用的常见生物学过程。
关键词: 活性氧生成,氧化应激,血管内皮功能障碍,抗氧化剂,血管收缩,血管扩张。
图形摘要
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