Enalaprilat reverses neutrophil polarization imbalance via targeting taurine-STING axis for treatment of diabetic wounds.
basic_science · Level V
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- Record sourced from PubMed, PMID 41916295.
- Also identified by DOI 10.1016/j.xcrm.2026.102714.
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Abstract
Persistent inflammation derived from neutrophil activation drives delayed healing of diabetic wounds. Herein, a dissolvable alginate methacryloyl-based microneedle patch functionalized with polypeptide CFLFLFK-NH<sub>2</sub>-coupled manganese/zinc ion metal-organic framework (MnZn-MOF) loading enalaprilat (Ena) (TMZE@A-MN) is developed. Ena promotes neutrophil repolarization from pro-inflammatory N1 to anti-inflammatory N2 state by inhibiting nuclear factor (NF)-κB axis and activating Smad3 pathway, attributed to Ena-induced level elevation of taurine and subsequently STING signaling cascade suppression, thus causing macrophage phenotype switching and endothelial cell ferroptosis repression. Due to identifiable property of CFLFLFK-NH2 on neutrophil membrane receptors, the delivery system endows Ena with targeting inhibitory roles in neutrophil activation. In addition, MnZn-MOFs possess free radical-eliminating performance and can effectively combat the growth of methicillin-resistant Staphylococcus aureus and Escherichia coli. In vivo evaluation on diabetic murine and porcine wounds also demonstrates that the TMZE@A-MN accelerates wound healing process. Consequently, the targeted microneedle delivery system holds great promise for diabetic wound treatment.