Background: Keloid is the result of abnormal hyperplasia of skin connective tissue. This study explored the relationship between m6A related genes and keloid, and provides some reference for discovering the pathogenesis and therapeutic targets of keloid. Methods: Transcriptomic datasets (GSE44270, GSE185309) of keloid and normal skin tissues were obtained from the Gene Expression Omnibus database (GEO). The landscape of m6A gene was constructed, then the corresponding genes were verified by immunohistochemistry. Using protein-protein interaction (PPI) network analysis, hub genes were extracted for unsupervised clustering analysis, and Gene ontology (GO) enrichment analysis was carried out to check the biological process or function affected by these differentially expressed genes. Finally, immune infiltration analysis was carried out to discuss the relationship between the therapeutic potential of keloid and immune microenvironment. Results: There were genes with different expression trends in the three types of m6A genes, especially IGF2BP3 in the reader category, which is significantly up-regulated in keloid patients. We identified 6 genes showed significant differences through PPI analysis between the two groups of keloid samples. Enrichment analysis was performed to identify the functions of these differentially expressed genes, and we found that they were related to cell division, proliferation and metabolism, and there were significant differences in immunity-related pathways. Finally, we analyzed the immune infiltration level of immune cells in keloid with single sample Gene Set Enrichment Analysis（ssGSEA）and CIBERSORT respectively. Conclusions: We analyzed the relationship between m6A related genes and keloid through bioinformatics methods, so as to provide corresponding references for clarifying the molecular mechanism of keloid.

The serve burn or scald wounds always face persistent infections and self-repair function decline caused by serious tissue necrosis, leading to delayed healing or even sepsis. In this work, we proposed a click-chemistry hydrogel delivery system of antibacterial and tissue remodeling function nanovesicles for deep scald wound treatment. An hydrophilic photodynamic aggregation-induced emission photosensitizer 4-(2-(5-(4-(diphenylamino)phenyl)thiophen-2-yl)vinyl)-1-(2-hydroxyethyl) pyridin-1-ium bromide (THB) was firstly encapsulated into nanovesicles derived from easily accessible adipose stem cells (ANVs) to create THB@ANVs, which exhibits enhanced bacteria-targeting property and multiple tissue remodeling effects. To deliver THB@ANVs, an injectable click-chemistry hydrogel of carboxymethyl chitosan was used to form a wound treatment system for deep scald wounds. The hydrogel can well matching the wound morphology and respond to the acidic microenvironment of the wound to accelerate sustained release. In vivo wound healing evaluations show that the composite hydrogel can efficiently accelerate wound healing by reducing the number of bacteria, promoting early angiogenesis, and regulating immune reaction. This study provides a simple, low-cost, and effective “one-stop” strategy with diverse functions and wide applicability for scald wound remodeling and antibiosis.

Owing to the persistent inflammatory microenvironment and unsubstantial dermal tissues, chronic diabetic wounds do not heal easily and their recurrence rate is high. Therefore, a dermal substitute that can induce rapid tissue regeneration and inhibit scar formation is urgently required to address this concern. In this study, we established biologically active dermal substitutes (BADS) by combining novel animal tissue‐derived collagen dermal‐replacement scaffolds (CDRS) and bone marrow mesenchymal stem cells (BMSCs) for the healing and recurrence treatments of chronic diabetic wounds. The collagen scaffolds derived from bovine skin (CBS) displayed good physicochemical properties and superior biocompatibility. CBS loaded with BMSCs (CBS‐MCSs) could inhibit M1 macrophage polarization in vitro. Decreased MMP‐9 and increased Col3 at the protein level were detected in CBS‐MSCs‐treated M1 macrophages, which may be attributed to the suppression of the TNF‐α/NF‐κB signaling pathway (downregulating phospho‐IKKα/β/total IKKα/β, phospho‐IκB/total IκB, and phospho‐NFκB/total NFκB) in M1 macrophages. Moreover, CBS‐MSCs could benefit the transformation of M1 (downregulating iNOS) to M2 (upregulating CD206) macrophages. Wound‐healing evaluations demonstrated that CBS‐MSCs regulated the polarization of macrophages and the balance of inflammatory factors (pro‐inflammatory: IL‐1β, TNF‐α, and MMP‐9; anti‐inflammatory: IL‐10 and TGF‐β3) in db/db mice. Furthermore, CBS‐MSCs facilitated the noncontractile and re‐epithelialized processes, granulation tissue regeneration, and neovascularization of chronic diabetic wounds. Thus, CBS‐MSCs have a potential value for clinical application in promoting the healing of chronic diabetic wounds and preventing the recurrence of ulcers.