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Chronic diabetic wounds are trapped in a self‐perpetuating vicious cycle—persistent infection, oxidative stress, and NET‐driven inflammation—that severely impairs healing. Here, we engineer a piezoelectric nanofiber membrane (DMTP) that breaks this cycle via a dynamic‐static dual‐mode strategy. DMTP integrates a Mn‐Ti bimetallic MOF with sustained DNase I release, enabling four coordinated functions: (i) piezodynamic ROS generation for on‐demand antibacterial action; (ii) an electric field to guide fibroblast migration; (iii) sustained DNase I release to degrade pathological NETs; and (iv) intrinsic POD/SOD enzyme‐mimetic activity for continuous ROS scavenging. Mechanistically, we show that NETs drive fibroblast differentiation into α‐SMA + myofibroblasts, a key fibrotic driver, and DMTP effectively suppresses this pro‐fibrotic process. In diabetic mice, DMTP achieves 94.32% wound closure with orderly collagen deposition and modulated inflammation (TNF‐α↓, TGF‐β↑). In a rabbit ear hypertrophic scar model, DMTP significantly reduces scar formation by inhibiting α‐SMA expression. This work offers a transformative strategy to achieve diabetic wound healing with diminished scarring by directly dismantling the infection–oxidative stress–NETs–fibrosis axis.
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Chen et al. (2026) studied this question.
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