Preventing Glioblastoma Relapse by Igniting Innate Immunity through Mitochondrial Stress in the Surgical Cavity

Preventing Glioblastoma Relapse by Igniting Innate Immunity through Mitochondrial Stress in the Surgical Cavity

© 2025 Wiley‐VCH GmbH.

Bibliographische Detailangaben
Veröffentlicht in:Advanced materials (Deerfield Beach, Fla.). - 1998. - (2025) vom: 08. Sept., Seite e11351
1. Verfasser: Han, Xu (VerfasserIn)
Weitere Verfasser: Feng, Fan, Wang, Zixu, Huang, Shujun, Xi, Kaiyan, Fang, Zezheng, Shen, Jianyu, Wang, Mingrui, Zhang, Yi, Liu, Ben, Wang, Junpeng, Wang, Jiahao, Liang, Xiangjun, Sun, Guangpan, Zhang, Runlu, Han, Baoteng, Liu, Fanlin, Li, Mingze, Zhang, Xun, Wang, Jingjing, Geng, Huimin, Zhang, Yanrong, Zhang, Wenli, Wu, Zimei, Li, Xingang, Li, Yi, Cheng, Lian, Zhang, Yulin, Ni, Shilei
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2025
Zugriff auf das übergeordnete Werk:Advanced materials (Deerfield Beach, Fla.)
Schlagworte:Journal Article charge‐reversal biomimetic nanoparticles glioblastoma innate Immunity mitochondrial stress tumor treating fields
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520 |a Innate immunity is crucial in orchestrating the brain immune response, however, glioblastoma multiforme (GBM) has evolved sophisticated mechanisms to evade innate immune surveillance, posing significant challenges for current immunotherapies. Here, a therapeutic strategy is reported that aims at reactivating innate immune responses in GBM via targeted induction of mitochondrial stress, thereby enhancing tumor immunogenicity. Specifically, innate immune-stimulating nanoparticles (INSTNA) are developed, encapsulating positively charged iridium-based complexes (Ir-mito) and small interfering RNA against Methylation-Controlled J protein (si-MCJ) to attenuate mitochondrial respiration. This combination effectively disrupts mitochondrial function of GBM cells, particularly when combined with tumor-treating fields. The engineered charge-reversal INSTNA impair the mitochondrial electron transport chain (ETC), inducing oxidative phosphorylation (OXPHOS) stress and subsequent mitochondrial matrix release. Furthermore, hydrogel-mediated delivery of INSTNA in a postoperative GBM mouse model significantly remodeled the immunosuppressive microenvironment, resulting in pronounced tumor regression. In sum, these findings highlight that targeted induction of mitochondrial stress in postoperative GBM can potentiate innate immune activation and enhance adaptive immunity, offering a promising avenue for mitigating GBM recurrence 
650 4 |a Journal Article 
650 4 |a charge‐reversal biomimetic nanoparticles 
650 4 |a glioblastoma 
650 4 |a innate Immunity 
650 4 |a mitochondrial stress 
650 4 |a tumor treating fields 
700 1 |a Feng, Fan  |e verfasserin  |4 aut 
700 1 |a Wang, Zixu  |e verfasserin  |4 aut 
700 1 |a Huang, Shujun  |e verfasserin  |4 aut 
700 1 |a Xi, Kaiyan  |e verfasserin  |4 aut 
700 1 |a Fang, Zezheng  |e verfasserin  |4 aut 
700 1 |a Shen, Jianyu  |e verfasserin  |4 aut 
700 1 |a Wang, Mingrui  |e verfasserin  |4 aut 
700 1 |a Zhang, Yi  |e verfasserin  |4 aut 
700 1 |a Liu, Ben  |e verfasserin  |4 aut 
700 1 |a Wang, Junpeng  |e verfasserin  |4 aut 
700 1 |a Wang, Jiahao  |e verfasserin  |4 aut 
700 1 |a Liang, Xiangjun  |e verfasserin  |4 aut 
700 1 |a Sun, Guangpan  |e verfasserin  |4 aut 
700 1 |a Zhang, Runlu  |e verfasserin  |4 aut 
700 1 |a Han, Baoteng  |e verfasserin  |4 aut 
700 1 |a Liu, Fanlin  |e verfasserin  |4 aut 
700 1 |a Li, Mingze  |e verfasserin  |4 aut 
700 1 |a Zhang, Xun  |e verfasserin  |4 aut 
700 1 |a Wang, Jingjing  |e verfasserin  |4 aut 
700 1 |a Geng, Huimin  |e verfasserin  |4 aut 
700 1 |a Zhang, Yanrong  |e verfasserin  |4 aut 
700 1 |a Zhang, Wenli  |e verfasserin  |4 aut 
700 1 |a Wu, Zimei  |e verfasserin  |4 aut 
700 1 |a Li, Xingang  |e verfasserin  |4 aut 
700 1 |a Li, Yi  |e verfasserin  |4 aut 
700 1 |a Cheng, Lian  |e verfasserin  |4 aut 
700 1 |a Zhang, Yulin  |e verfasserin  |4 aut 
700 1 |a Ni, Shilei  |e verfasserin  |4 aut 
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