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上调的化修饰通过改变线粒体能量代谢来诱导微质中的衰老表型

Xinnan Zhao¹, Xiaohan Yang^1,2, Cong Du¹

¹Department of Anatomy, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China.

Journal of neuroinflammation

|November 15, 2024

概括

增加化,一种代谢变化,通过改变能量路径,驱动微质细胞衰老和神经炎症. 降低化水平可能为与年龄相关的神经退行性疾病提供新的治疗方法.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
生物化学生化学

背景情况:

中枢神经系统 (CNS) 的衰老有助于神经退行性疾病.
神经炎症,包括微质 (MG) 激活和细胞因子,与神经退行有关.
微质激活是通过代谢重编程来调节的,但 succinylation 的作用是未知的.

研究的目的:

研究化在微质激活和衰老中的作用.
确定化是否影响线粒体功能和微质中的能量代谢.
探索化作为与衰老相关的神经炎症的治疗点.

主要方法:

测量了老化和脂聚糖 (LPS) 激活的微质中的化水平.
在BV2微质细胞中利用sirtuin 5 knockdown (Sirt5 KD) 诱导化.
评估了线粒体功能,基因表达,活性氧物种 (ROS) 和脂质过氧化.
采用免疫沉和酶活性测试来研究化对线粒体酶的影响.
施用酸酸 (SP) 在体外和体内降低酸的调节.

主要成果:

随着年龄的增长和LPS诱导的MG激活,糖化水平增加.
Sirt5 KD提升了化,导致与衰老相关的基因上调,线粒体适应能力受损,并转向糖解.
用LPS治疗的Sirt5 KD BV2细胞显示ROS增加,脂质滴积累和脂质过氧化.
已经证明,糖化可以调节像SDH和ECHA这样的线粒体酶.
SP治疗减少了MG衰老和神经炎症.

结论:

上调的化促进微质衰老通过改变能量代谢.
糖化修饰在线粒体酶活性中起着调节作用.
向化水平为与衰老相关的神经炎症和神经退行性疾病的潜在治疗策略.

关键词:

衰老的衰老衰老的衰老代谢重编程是一种代谢重编程.微质细胞中的微质细胞神经炎症是一种神经炎症.糖化 (Succinylation) 是一种作用.

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