在老年心脏中,Endoplasmic网膜应激和氧素的变化
Qun Chen1, Jeremy Thompson1, Ying Hu1
1Departments of Medicine (Division of Cardiology), Virginia Commonwealth University, Richmond, VA 23298, USA.
Mechanisms of ageing and development
|September 3, 2023
概括
衰老会增加氧化应激,并损害抗氧化防御,如百氧化素3 (PRDX3) 通过引起内质网膜 (ER) 应激. 减少ER压力有助于恢复老年心脏中的PRDX3水平.
科学领域:
- 心血管生物学 心血管生物学
- 衰老研究研究 衰老研究
- 氧化应激机制 氧化应激机制
背景情况:
- 与衰老相关的心血管疾病与氧化压力有关.
- 细胞内膜网膜 (ER) 的压力加剧了氧化压力,并在衰老过程中损害了线粒体功能.
- 降低抗氧化剂水平,如过氧化素 (PRDXs),加剧了衰老中的氧化应激.
研究的目的:
- 为了研究ER应激和过氧化 (PRDX) 在衰老过程中的降解之间的关系.
- 确定ER压力是否有助于老年心脏中氧化压力的增加.
- 评估ER应激缓解对PRDX水平和老年小鼠氧化应激的影响.
主要方法:
- 年轻成年人 (3月) 的比较. 和老年 (24 个月). 雄性小鼠.雄性小鼠.
- 用4-丁酸 (4-PBA) 治疗以缓解ER压力.
- 测量心脏组织中氧化应激水平,PRDX3 (线粒体) 和PRDX4 (心肌) 含量.
主要成果:
- 老年心脏的氧化压力比年轻的心脏高.
- 4-PBA治疗减少了老年心脏的氧化应激,证实了ER应激的作用.
- 衰老导致PRDX3和PRDX4水平下降;4-PBA改善了PRDX3,但没有改善PRDX4含量.
结论:
- 在老化过程中,ER压力导致线粒体功能障碍和氧化应激增加.
- 通过降低PRDX3水平,ER压力会损害抗氧化剂防御.
- 在衰老过程中,PRDX4可能在ER应激诱导中发挥上游作用.
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