ArticleMaterials today. Bio2026
A nanozyme-augmented peripheral nerve-targeting liposome alleviates local immune inflammation and ferroptosis for enhanced facial nerve repair.
Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Facial nerve injury (FNI) is a common form of peripheral nerve damage that often results in incomplete functional recovery due to a hostile microenvironment characterized by excessive oxidative stress and inflammatory activation. These pathological conditions disrupt Schwann cell homeostasis, impair myelin maintenance, and hinder nerve regeneration. Although ferroptosis, an iron-dependent lipid peroxidation-driven form of regulated cell death, has been implicated in peripheral nerve disorders, its involvement in acute FNI remains not fully defined. In this study, transcriptomic analysis of injured facial nerve tissue suggested ferroptosis-related transcriptional alterations and lipid peroxidation-associated cellular injury during the acute phase of FNI, including changes in ferroptosis-related gene expression, decreased GPX4 levels, and increased 4-HNE accumulation. To modulate this complex microenvironment, we developed a peripheral nerve-targeted, ROS-responsive liposomal nanoplatform (F-MHC@PNRLs) co-delivering Ferrostatin-1 (Fer-1) and Mn-doped CeO
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