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CALCOCO2通过调节线粒细胞衰变和线粒体应激之间的相互作用来防止AngII诱导的心房重塑

Wanyue Sang¹, Xiaoji Yan², Lu Wang¹

¹Cardiac Pacing and Electrophysiology Department, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China; Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.

International immunopharmacology

|August 2, 2024

概括

结合和卷曲-卷曲域2 (CALCOCO2) 通过增强线粒细胞衰变和减少线粒体应激,防止心房动 (AF). 过度表达CALCO2可逆转AF诱导的心房重塑,提供一个潜在的治疗点.

科学领域:

心脏病学心脏病学
线粒体生物学线粒体生物学
细胞应激反应的应激反应

背景情况:

线粒体功能障碍与心房动 (AF) 病变发生有关.
结合和卷轴-卷轴域2 (CALCOCO2) 是一个有机受体,在AF中起着未知的作用.
这项研究调查了CALCOCO2在AF中的功能,重点关注线粒体和线粒体应激.

研究的目的:

阐明CALCOCO2在心房动 (AF) 中的作用和分子机制.
在AF模型中确定CALCOCO2对线粒体和线粒体应激的调节作用.

主要方法:

在小鼠和HL-1细胞中使用AngII治疗建立了体外和体外AF模型.
评估了CALCOCO2和DAP3结合细胞死亡增强剂1 (DELE1) 过度表达对线粒体和线粒体应激的影响.
利用诺基因抑制线粒细胞衰变,并研究其在CALCOCO2影响中的作用.
通过光探针,电子显微镜,西部涂抹,免疫组织化学和共聚焦显微镜分析线粒体参数.

主要成果:

在AF模型中,AngII诱导了线粒体损伤,抑制了线粒体,并促进了心房重塑.
过度表达CALCOCO2改善了AF诱导的线粒体功能障碍,纤维化和氧化应激.
CALCOCO2通过激活线粒体和减轻线粒体压力来恢复线粒体平衡.
过度表达DELE1加剧了线粒体的活性氧物种和压力蛋白表达,即使存在CALCOCO2.

结论:

CALCOCO2通过调节线粒体和DELE1介导的线粒体应激,在AF中发挥保护作用.
在AF中,CALCOCO2代表了预防或逆转心房重塑的潜在治疗标.
准CALCOCO2可能为AF治疗提供一种新的策略.

关键词:

英语英语英语英语英语英语心房动是一种心房动.在心房重塑.这就是CALCOCO2的含量.线粒体应激压力是什么线粒细胞衰变 (mitophagy) 是一种神经衰变.

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