Charge‐Driven Bioshield Remodels Diabetic Oral Microenvironment for Accelerated Wound Healing

Diabetic chronic wounds, especially in the moist and mechanically dynamic oral environment, pose a significant therapeutic challenge due to neutrophil extracellular traps (NETs)-mediated inflammation, biofilm infections, and extracellular matrix remodeling defects. To address this challenge, we develop a protein-based adhesive bioshield, functioning through the combined action of physical blocking and electrostatic interaction, that simultaneously acts as a bacterial barrier and NETs scavenger, thereby reactivating the focal adhesion signaling. The protein's high-density lysine residues establish a robust adhesion network that resists the dynamic oral environment while creating a persistent antibacterial bioshield. Notably, the high net charge of adhesive bioshield enables rapid NETs neutralization by electrostatically binding cell-free DNA (cfDNA), which reduces local NETs levels and inflammatory responses. This NETs clearance subsequently alleviates inflammation-mediated suppression of focal adhesion signaling, which coordinately accelerates diabetic wound healing through enhanced epithelial migration, endothelial proliferation, and angiogenesis. Overall, this study presents a charge-driven therapeutic strategy that targets NETs-mediated inflammation, offering an alternative approach for managing diabetic wounds in dynamic and wet environments.

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Publication Details

Journal
Advanced Materials
Published
2026-01-02
DOI
https://doi.org/10.1002/adma.202516778
Primary Topic
Wound Healing and Treatments
Type
article
Field-Weighted Citation Impact
0.00

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article

Charge‐Driven Bioshield Remodels Diabetic Oral Microenvironment for Accelerated Wound Healing

Hongjie Zhang, Yajuan Xie, Yusai Zhou, Xiaomo Liu et al.
Advanced Materials
Wound Healing and Treatments
article

Charge‐Driven Bioshield Remodels Diabetic Oral Microenvironment for Accelerated Wound Healing

Hongjie Zhang, Yajuan Xie, Yusai Zhou, Xiaomo Liu, Ruichu Zhang, Bo Li, Y F Yang, Yabo Wang, Yunfan Zhang, Yan Wei, Bing Han, Chao Ma, Kai Liu
article en

Abstract

Diabetic chronic wounds, especially in the moist and mechanically dynamic oral environment, pose a significant therapeutic challenge due to neutrophil extracellular traps (NETs)-mediated inflammation, biofilm infections, and extracellular matrix remodeling defects. To address this challenge, we develop a protein-based adhesive bioshield, functioning through the combined action of physical blocking and electrostatic interaction, that simultaneously acts as a bacterial barrier and NETs scavenger, thereby reactivating the focal adhesion signaling. The protein's high-density lysine residues establish a robust adhesion network that resists the dynamic oral environment while creating a persistent antibacterial bioshield. Notably, the high net charge of adhesive bioshield enables rapid NETs neutralization by electrostatically binding cell-free DNA (cfDNA), which reduces local NETs levels and inflammatory responses. This NETs clearance subsequently alleviates inflammation-mediated suppression of focal adhesion signaling, which coordinately accelerates diabetic wound healing through enhanced epithelial migration, endothelial proliferation, and angiogenesis. Overall, this study presents a charge-driven therapeutic strategy that targets NETs-mediated inflammation, offering an alternative approach for managing diabetic wounds in dynamic and wet environments.

Advanced MaterialsVol. 38(11)
King University (US), Peking University (CN), Jiaxing University (CN), Peking University People's Hospital (CN), Peking University First Hospital (CN), Stomatology Hospital (CN), Ministry of Education (TW), Tsinghua University (CN)
National Natural Science Foundation of China, Chinese Academy of Sciences, China Postdoctoral Science Foundation, Ministry of Health of the People's Republic of China, University of Chinese Academy of Sciences, Wenzhou Institute of Biomaterials and Engineering
Openalex Percentile: Top 98%
Wound Healing and Treatments
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