Exosomes derived from fibroblasts in DFUs delay wound healing by delivering miR-93-5p to target macrophage ATG16L1.

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Tác giả: Weicheng Gao, Jinde Lin, Tianyi Ni, Xiaowei Sun, Liying Tu, Guoping Wu, Zibo Xu, Wei Yan, Min Yi, Lantian Zhang, Qian Zhang, Liping Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 573.1556 *Circulatory system

Thông tin xuất bản: Netherlands : Biochimica et biophysica acta. Molecular basis of disease , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 189916

Diabetes is an extremely costly disease, one-third of which are attributed to the management of diabetic foot disease including chronic, non-healing, diabetic foot ulcers (DFUs). Therefore, much effort is needed to understand the pathogenesis of DFUs and novel therapeutics. We utilized exosome staining to confirm the interaction between fibroblast-derived exosomes and macrophages. Subsequently, we employed public data and qPCR to screen for upregulated miRNAs in fibroblast-derived exosomes in DFUs. The relationship between was validate miR-93-5 and ATG16L1 through data prediction and dual-luciferase reporter assays. A variety of molecular biology experiments were used for subsequent pathway validation. Additionally, we established Atg16l1
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