biostudies-literatureLi FXHealth Research Project of Hunan Provincial Health CommissionNational Key Research & Development ProgramThe Health Research Project in Hunan ProvinceNational Key Research & Development Programthe Natural Science Foundation of Hunan ProvinceNational Clinical Key Specialties Major Research Projectsthe Scientific Research Launch Project for new employees of the Second Xiangya Hospital of Central South Universitythe National Natural Science Foundation of China723https://www.ebi.ac.uk/biostudies/studies/S-EPMC11577949biostudies-literatureUnknown22(1)Cold temperatures have been shown to slow skin wound healing. However, the specific mechanisms underlying cold-induced impairment of wound healing remain unclear. Here, we demonstrate that small extracellular vesicles derived from cold-exposed mouse plasma (CT-sEVs) decelerate re-epithelialization, increase scar width, and weaken angiogenesis. CT-sEVs are enriched with miRNAs involved in the regulation of wound healing-related biological processes. Functional assays revealed that miR-423-3p, enriched in CT-sEVs, acts as a critical mediator in cold-induced impairment of angiogenic responses and poor wound healing by inhibiting phosphatase and poly(A) binding protein cytoplasmic 1 (PABPC1). These findings indicate that cold delays wound healing via miR-423-3p in plasma-derived sEVs through tJournal of nanobiotechnologyMechanism of cold exposure delaying wound healing in mice.PMC11577949823708927673W202430192022JJ407212021YFC2501701Z202302620231696Zheng MHLiu JJCao YCYuan LQLin XTang KXDuan JYLi FXXu FWu YLHe SYLi YHWu FShan SKChen XCui RRGuo BLi CCWu YYLei LMfalseMechanism of cold exposure delaying wound healing in mice.Cold temperatures have been shown to slow skin wound healing. However, the specific mechanisms underlying cold-induced impairment of wound healing remain unclear. Here, we demonstrate that small extracellular vesicles derived from cold-exposed mouse plasma (CT-sEVs) decelerate re-epithelialization, increase scar width, and weaken angiogenesis. CT-sEVs are enriched with miRNAs involved in the regulation of wound healing-related biological processes. Functional assays revealed that miR-423-3p, enriched in CT-sEVs, acts as a critical mediator in cold-induced impairment of angiogenic responses and poor wound healing by inhibiting phosphatase and poly(A) binding protein cytoplasmic 1 (PABPC1). These findings indicate that cold delays wound healing via miR-423-3p in plasma-derived sEVs through t2024-01-01T00:00:00Z2024 Nov2025-04-19T14:35:36.445Z2025-04-19T14:35:36.445ZS-EPMC115779493956800210.1186/s12951-024-03009-y