细胞生物学
巨噬细胞
线粒体生物发生
重编程
线粒体ROS
活性氧
蛋白激酶B
化学
促炎细胞因子
PI3K/AKT/mTOR通路
伤口愈合
甘露糖受体
线粒体
氧化应激
腺苷
下调和上调
M2巨噬细胞
巨噬细胞极化
免疫系统
再生(生物学)
癌症研究
细胞因子
基因敲除
炎症
药理学
作者
Ganghua Yang,Jianqiu Yang,Zhaoping Diao,Jiajun Long,Zhiwen Shu,C J Liu,Wenjun Wan
出处
期刊:Science Advances
[American Association for the Advancement of Science]
日期:2025-10-31
卷期号:11 (44): eadw3834-eadw3834
被引量:18
标识
DOI:10.1126/sciadv.adw3834
摘要
Precise macrophage modulation is essential for diabetic wound treatment, yet mitochondrial dysfunction often sustains proinflammatory states. We developed cascade-targeting nanoparticles [epigallocatechin-3-gallate and metformin nanoparticles modified with mannose (EM/Man NPs)] to regulate macrophage mitochondria, integrated into a detachable core-shell microneedle patch (EM/Man MNs) made of quaternary ammonium chitosan and reactive oxygen species (ROS)-degradable polymer. The patch offered high penetration and antibacterial activity, while its ROS-sensitive core released EM/Man NPs to scavenge ROS, restore adenosine 5'-triphosphate production, and reestablish redox balance. The NPs further activated the adenosine 5'-monophosphate-activated protein kinase/Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1α axis to promote mitochondrial biogenesis and oxidative phosphorylation, repolarizing macrophages to an anti-inflammatory phenotype. In diabetic mice, EM/Man MNs accelerated healing via bacterial clearance, immune reprogramming, angiogenesis, and collagen deposition while inhibiting scar formation through interleukin-17 and phosphatidylinositol 3-kinase-Akt suppression. This cascade-targeting strategy for modulating macrophage mitochondria to regulate immunity and redox homeostasis provides a previously unidentified approach for designing tissue engineering materials.
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