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离子通过TRPM2通道调节对单细胞子组进行重新编程,以增强骨质整合

Congrui Zhao^1,2, Antian Xu^1,2, Jingyao Gong^1,2

¹Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, Hangzhou 310000, China.

Biomaterials research

|November 26, 2025

概括

用添加的植入物重编程称为单细胞的免疫细胞,减少炎症并改善植入物周围的骨愈合. 这种基于材料的免疫调节通过向TRPM2-NLRP3途径来增强骨整合.

科学领域:

生物材料科学生物材料科学
免疫学免疫学免疫学
整形外科工程整形外科工程

背景情况:

成功的骨质整合需要在生物材料-组织接口的早期免疫恒常状态.
用 (Sr) 修饰的生物材料有望增强骨质整合,但它们对单细胞的免疫调节作用尚不清楚.
了解Sr对单细胞子集的影响对于设计有效的生物材料至关重要.

研究的目的:

研究工程植入物的局部释放如何重编程单细胞子集.
阐明中介免疫调节的潜在分子机制.
评估这些变化对骨质整合和骨再生的影响.

主要方法:

工程化石合剂喷砂,大砂和酸蚀刻 (Sr-SLA) 植入物.
单细胞RNA测序以分析植入物周围的单细胞子集动态.
在体外验证离子对单细胞炎症酶激活 (TRPM2-NLRP3轴) 和细胞因子概况的影响.
在体内研究评估与或没有单细胞枯竭的骨质整合.

主要成果:

Sr-SLA植入物创造了一个抗炎微环境,促进骨质整合.
通过抑制TRPM2-Ca2+-NLRP3炎症酶通路,Sr-SLA抑制了亲炎症的经典单细胞 (Ly6C).
Sr-SLA促进了再生的非古典单细胞 (Ly6C^lo),从而产生了增强骨髓中酶体 stromal 细胞骨质分化的细胞因子特征.
单细胞枯竭在体内显著损害了骨质整合.

结论:

Sr-SLA植入物通过TRPM2-Ca2+-NLRP3轴有效地重编程单细胞子集,减少炎症并增强骨再生.
这项研究将生物材料特性与免疫反应和骨愈合联系起来,确定了免疫调节生物材料的可设计目标.
单细胞在植入物介导的骨再生中发挥着不可或缺的作用.

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