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缺血-再输液损伤诱导了内皮细胞中ZBP1-依赖的PANoptosis

Yue Cui¹, Huang Lin¹, Jiaxing Ma¹

¹Department of Aesthetic Plastic Surgery and Laser Medicine, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing 100029, China.

Biochimica et biophysica acta. Molecular basis of disease

|March 8, 2025

概括

缺血-反损伤 (IRI) 通过依赖于Z-结合蛋白1 (ZBP1) 的PANoptosome形成在内皮细胞中触发PANoptosis. 这项研究确定ZBP1是关键的调解者,为保护这些重要细胞提供了潜在的目标.

科学领域:

细胞生物学细胞生物学
病理生理学病理生理学
分子机制的分子机制

背景情况:

内皮细胞在缺血 - 反损伤 (IRI) 病理生理学中至关重要.
已知IRI会激活PANoptosis,但确切的机制尚未完全理解.

研究的目的:

研究IRI如何在内皮细胞中诱导PANoptosis.
确定潜在的保护策略,防止IRI诱导的PANoptosis.

主要方法:

已在体外内皮细胞低氧/低氧化 (H/R) 和体内大鼠自由 IRI 模型中建立.
使用PI/Hoechst染色,西式涂抹和免疫组织化学来评估细胞死亡.
采用ZBP1 siRNA转染和免疫沉来探索信号通路.

主要成果:

IRI激活了类似PANoptosis的细胞死亡,并在内皮细胞中调节了Z-结合蛋白1 (ZBP1) 的表达.
击败ZBP1显著改变了类似PANoptosis的细胞死亡和ZBP1-PANoptosome组装.
证实了由ZBP1.1介导的PANoptosis的发生.

结论:

在内皮细胞中,IRI诱导PANoptosome的形成.
ZBP1是IRI诱导的PANoptosis的一个关键媒介.
向ZBP1可能为内皮细胞中的IRI提供一种保护策略.

关键词:

内皮细胞内皮细胞的内皮细胞.缺血-再输液损伤缺血-再输液损伤这就是PANoptosis.Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA Z-NA 在 ZBP1 中,ZBP1 是

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