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热量过高会诱导小鼠巨细胞减少压力

Rong Xu¹, Xiu-Wen Liang², Qi-Hai Cai³

¹Department of Immunology and Microbiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China; State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.

Biochimica et biophysica acta. Molecular basis of disease

|December 11, 2025

概括

热应激通过减少应激而不是氧化应激导致细胞死亡 (PANoptosis),因为它会损害硫素 (Trx) 系统. 卡斯帕斯和RIPK3的双重抑制可以防止热冲击损伤.

科学领域:

细胞生物学细胞生物学
分子机制的分子机制
压力反应应激反应

背景情况:

过热引起的热应激 (HS) 会导致器官损伤和死亡.
HS诱导的细胞死亡的精确分子机制尚不清楚.
现有的研究往往侧重于氧化应激,忽视了其他促成因素.

研究的目的:

为了阐明宏细胞中HS诱导的细胞死亡的机制.
调查氧化压力与减少压力在HS诱导的PANoptosis中的作用.
为了确定HS相关疾病的潜在治疗点.

主要方法:

巨细胞培养受热应激的影响.
评估细胞死亡途径 (烧灭,灭,灭) 和PANoptosome的形成.
测量反应性氧物种 (ROS) 和还原性压力标志物 (NADPH,硫素系统).
药理上抑制卡斯帕斯和RIPK3.
在小鼠模型中对HS诱导的肠损伤进行体内验证.

主要成果:

HS诱导的PANoptosis独立于ROS,表明氧化应激不是主要的驱动因素.
HS导致了减少性压力,其特点是NADPH积累和硫素 (Trx) 系统功能障碍.
Trx1聚合损害了氧化还原调节,导致线粒体损伤和DNA损伤.
双重抑制卡斯帕斯 (IDN-6556) 和RIPK3 (GSK'872) 完全阻止了HS诱导的PANoptosis.
联合抑制保护在体内免受HS诱导的肠损伤.

结论:

降解性压力,由氧素系统功能障碍介导,是HS诱导的PANoptosis的关键驱动因素,而不是氧化压力.
针对caspases和RIPK3提供了一种针对热冲击相关病理的新治疗策略.
了解减轻性压力机制为治疗高热引起的器官损伤开辟了新的途径.

关键词:

热应激是一种热应激.巨细胞是一个巨细胞.线粒体损伤导致线粒体损伤.这就是PANoptosis.有反应性氧物种的反应性氧物种.减轻压力可以减少压力.

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