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YAP1通过促进BNIP3介导的线粒细胞衰变来加剧细胞核中的热和衰老

Xin Peng¹, Hang-Yu Ji², Jia-Wei Gao³

¹Department of Orthopedics, Henan Provincial People's Hospital, Peolple's Hospital of Zhengzhou University, Zhengzhou, China.

International immunopharmacology

|October 23, 2024

概括

是的相关蛋白1 (YAP1) 通过促进线粒细胞衰变,加剧炎症诱导的炎和衰老在细胞核中. 然而,YAP1可能为急性磁盘退行性损伤提供治疗潜力.

科学领域:

细胞生物学细胞生物学
生物化学生物化学
病理学病理学病理学

背景情况:

是的相关蛋白1 (YAP1) 是一个关键的Hippo通路效应因子,参与炎症和线粒体功能.
在炎症过程中,YAP1在细胞核核突 (NP) 细胞内的热致死和线性的作用尚未完全被理解.

研究的目的:

为了研究YAP1对NP细胞中脂聚糖 (LPS) 诱导的热的作用.
探索涉及线粒和炎症酶激活的潜在机制.

主要方法:

在NP细胞中过度表达YAP1.
用LPS诱导模拟炎症环境.
评估热,衰老,线粒 (BNIP3介导) 和炎症酶 (NLRP3) 激活.
在体内研究使用正常和annulus纤维状穿孔盘.

主要成果:

在退行性磁盘NP组织中,YAP1的表达减少.
过度表达YAP1加剧了LPS诱导的热,衰老和NLRP3炎症酶激活.
抑制BNIP3介导的线粒可以逆转YAP1诱导的热和衰老.
在体内,YAP1的过度表达加速了正常的磁盘退化,但减弱了状纤维突破性磁盘的退化.
YAP1的过度表达上调了TNFAIP3和CLPP.

结论:

YAP1通过促进BNIP3介导的线粒细胞衰变,加剧NP细胞中的LPS诱导的热和衰老,从而导致磁盘退化.
由于其在特定的体内模型中的保护作用,YAP1显示为急性椎间盘退化 (IDD) 损伤的治疗剂的潜力.

关键词:

炎症炎症是一种炎症.线粒细胞衰变 (mitophagy) 是一种神经衰变.在NLRP3中,NLRP3是NLRP3中的一个.它的核心是脉的.一个YAP1一个YAP1

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