化学
细胞生物学
伤口愈合
活性氧
细胞外基质
内皮干细胞
细胞外
下调和上调
血管生成
小泡
内皮
基质金属蛋白酶
巨噬细胞
细胞迁移
生长因子
内化
巨噬细胞极化
细胞生长
癌症研究
细胞内
细胞
氧化磷酸化
脐静脉
血管内皮生长因子
生物化学
作者
Sheng Ding,Siyu Liu,Chunxiao Zhou,Shuwei Wang,Rui Gao,Shaoyang Kang,Chuangnian Zhang,Pingsheng Huang,Wenshuai Liu,Zujian Feng,Deling Kong,Weiwei Wang
标识
DOI:10.1021/acsami.5c25922
摘要
, P-MG@vEVs efficiently scavenged ROS, modulated macrophage polarization toward the anti-inflammatory M2 phenotype, and enhanced angiogenesis. In streptozotocin (STZ)-induced diabetic mice, P-MG@vEVs efficiently reprogrammed the damaged cutaneous microenvironment via regulating key signaling pathways (e.g., HIF-1, IL-17, NF-κB), thereby alleviating inflammation, restoring redox homeostasis, and facilitating neovascularization. These multifaceted effects significantly accelerate wound closure and skin repair, as evidenced by enhanced re-epithelialization and improved collagen deposition. Collectively, this platform integrates the intrinsic bioactivity of VEGF-preconditioned vEVs with the ROS-responsive delivery capability of the microgel carrier, offering a highly promising strategy for diabetic wound management.
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