败血症
免疫系统
吞噬作用
炎症
钙
体内
药理学
抗体调理
癌症研究
生物学中的钙
细胞生物学
免疫学
医学
细胞内
生物
内科学
调理素
生物技术
作者
Peng Xiang,Mingyang Zhao,Yue He,Min Wang,Ping Yin,Tian Su
标识
DOI:10.1002/adhm.202501218
摘要
Abstract Disorders in Ca 2+ signaling contribute to many metabolic manifestations of sepsis and are one of the driving forces underlying multiorgan failur e. Herein, a compensatory elevation in calcium‐binding protein grancalcin (GCA) levels in monocytes and macrophages of patients and mice with sepsis is observed. Gca deletion in myeloid cells displays increased inflammation and organ damage in cecal ligation and puncture‐induced sepsis. Mechanistically, GCA enhances the phagocytic function of immune cells by regulating intracellular calcium signaling. A GCA@Acrylate‐PEG‐NHS/weakly temperature‐sensitive gelatin methacrylate (GelMA) microneedle patch (GCA@NHS/GelMA‐MNPs) is designed. In vivo experiments demonstrate that this patch establishes a sustained drug release mechanism, boosts the phagocytic capacity of immune cells, and improves sepsis outcomes by restoring Ca 2+ signaling homeostasis. These findings suggest that GCA‐loaded hydrogel microneedle patches can be a promising new treatment for sepsis.
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