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HDAC6/Trim21通过GSDMD信号通路加剧巨细胞的炎症反应和诱导的骨解

Junxi Chen¹, Taihe Liu¹, Jiankai Luo¹

¹Department of Orthopedic Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, PR China.

Journal of immunology (Baltimore, Md. : 1950)

|August 2, 2025

概括

基因组脱乙酶6 (HDAC6) 和三方基因含有蛋白21 (Trim21) 通过激活Gasdermin D (GSDMD) 信号来加剧无菌松动. 这一途径驱动巨细胞炎症和骨解,以应对颗粒.

科学领域:

生物医学工程生物医学工程
免疫学免疫学免疫学
整形外科手术整形外科手术

背景情况:

无菌松动是全关节关节整形手术的一个主要并发症.
假肢的磨损颗粒会激活巨细胞,导致骨质溶解.
在这个过程中,HDAC6,Trim21和GSDMD的作用需要进一步阐明.

研究的目的:

在磨损颗粒诱导的无菌松动中研究与GSDMD相关的信号通路的HDAC6/Trim21调节机制.
澄清HDAC6/Trim21在巨细胞激活和骨解中的体内和体外作用.

主要方法:

RAW264.7巨细胞与无菌颗粒 (TiP) 进行共同化.
使用了HDAC6抑制剂 (图巴斯丁A),HDAC6过度表达的林氏病毒和Trim21 siRNA.
建立了一个小鼠骨解剖模型来评估TiP诱导的骨解剖.

主要成果:

TiPs诱导了M1巨细胞两极分化,产生IL-1β和IFN-γ.
HDAC6与Trim21直接相互作用,通过GSDMD,STING和NLRP3通路促进炎症.
在体内,HDAC6加剧了TiP诱导的骨解和IL-1β产生.

结论:

HDAC6/Trim21信号加剧了巨细胞的炎症反应和诱导的骨解.
在这个过程中,GSDMD信号通路是关键的调解者.
针对HDAC6/Trim21/GSDMD可能为无菌松动提供治疗策略.

关键词:

GSDMDMD的总体发展目标是什么在 HDAC6 中.修剪2121 这是一个很好的方法.信号通道的信号通道.

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