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A frog bioactive peptide suppresses inflammation by modulating autophagy for skin wound regeneration
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DOI：10.1038/s42003-026-10766-z.png)
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Abstract
En 中文
Failure of inflammation resolution is a key driver of chronic skin wound pathogenesis, highlighting importance in wound healing. Although autophagy is known to regulate this process, it remains unclear whether amphibian-derived peptides exert their effects to facilitate regeneration of wounds through autophagy. Here, we identified OL-RA11, a previously unreported autophagy-regulatory peptide from Odorrana livida, which exhibits potent therapeutic effects on skin wounds. Mechanistically, OL-RA11 promoted wound healing through a dual cell-type-specific mechanism. During the early inflammatory stage, OL-RA11 enhanced autophagy in macrophages, which in turn induced M2 polarization and suppressed pro-inflammatory cytokine expression, thereby enabling inflammation resolution and facilitating the transition to the proliferative stage. In the proliferative phase, OL-RA11 directly activated the Wnt pathway in keratinocytes to enhance cell migration and promote re-epithelialization. Through this dual mechanism, autophagy and Wnt signaling acted independently in distinct cell types to coordinate inflammation resolution with regenerative activation, which ensured efficient, high-quality wound healing. A frog-derived peptide OL-RA11 promotes skin wound healing by inhibiting inflammation through autophagy modulation and accelerating re-epithelialization
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