Burns & Trauma最新文献

{"title":"Single cell deciphering of pruritic keloids: the interaction between fibroblasts and Schwann cells through the Midkine signaling","authors":"En Yang, Ruoqing Xu, Liying Tu, Hanrui Zhang, Shenying Luo, Hsin Liang, Yunhan Liu, Shuchen Gu, Yixuan Zhao, Xin Huang, Tao Zan","doi":"10.1093/burnst/tkaf057","DOIUrl":"https://doi.org/10.1093/burnst/tkaf057","url":null,"abstract":"Background Keloids are a common skin fibroproliferative disease that can result in severe aesthetic and functional concerns. Pruritus and pain are the most prevalent clinical manifestations of keloids. Schwann cells (SCs) variation and neuropathy within keloids contribute to these uncomfortable sensations; however the underlying mechanisms remain unclear. Objectives To explore the potential role of fibroblasts (FBs) and SCs in pruritic and pain keloids. Methods The activity of FBs and SCs was investigated using single-cell RNA sequencing (scRNA-seq) data of keloids. These bioinformatics analysis results were validated through in vitro cell culture, clinical samples, and in vivo experiments. The selected molecule was confirmed to be correlated with pain and itch and was subsequently used to treat cells in order to investigate its role in keloids. The in vivo inhibition assay was performed to evaluate its therapeutic potential. Results Our scRNA-seq analysis identified specific types of FBs and SCs were present in higher proportions in keloids and exhibited neurogenesis-related functions. Upon conducting an interaction analysis of these two cell types, we identified a critical molecule, Midkine (MDK), which is positively correlated with the patients’ pain and itching levels. Besides, MDK treatment facilitated the proliferation of SCs and their transition to a repairing phenotype, resulting in neuronal axonogenesis. This activation of repairing SCs promoted the release of substance P from nerve fibers, leading to clinical symptoms of pain and pruritus in keloid patients. Targeting MDK effectively reduces abnormal Schwann cell proliferation and subsequently inhibits the secretion of neuropeptides that trigger pain and pruritus. Conclusion Our study uncovered the interaction between FBs and SCs in the development of keloidal pain and pruritus, offering a novel therapeutic strategy to alleviate the distressing symptoms of keloids.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"28 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone Lactylation Exacerbates Acute Lung Injury in Septic Mice by Promoting Ferroptosis in Pulmonary Microvascular Endothelial Cells","authors":"Pu Fang, Shuai Li, Zong-Qing Lu, Dun-Lin Xia, Meng-meng Xu, Jingjing Pan, Lin Fu, Geng-Yun Sun, Qing-Hai You","doi":"10.1093/burnst/tkaf056","DOIUrl":"https://doi.org/10.1093/burnst/tkaf056","url":null,"abstract":"Background: Circulating lactate is associated with poor prognosis in sepsis-induced acute lung injury (S-ALI). However, it remains unclear whether microvascular dysfunction, a hallmark of S-ALI, is related to circulating lactate levels and what the underlying mechanisms are. The aim of this study was to investigate the role and mechanisms of lactate in pulmonary microvascular dysfunction in S-ALI. Methods: The effects of lactate on pulmonary microvascular function were assessed in a septic mouse model. Primary mouse pulmonary microvascular endothelial cells (MPMVECs) were isolated to evaluate the impact of lactate on MPMVEC permeability. Transcriptomic sequencing was employed to investigate the involvement of lactate in regulating MPMVEC ferroptosis, and the results were validated by in vivo and in vitro experiments. Histone lactylation was identified as a regulator of lipid peroxidation and iron homeostasis dysregulation in lactate-induced ferroptosis in MPMVECs. Gain- and loss-of-function approaches were used to assess the role of histone lactylation in regulating ferroptosis and pulmonary microvascular dysfunction. Correlations between serum lactate and ferroptosis levels and their associations with patient prognosis were investigated in patients with sepsis-associated acute respiratory distress syndrome (S-ARDS). Results: The mouse serum lactate level reached a peak at 18 hours after caecal ligation and puncture surgery. Elevated lactate levels during sepsis promoted ferroptosis in PMVECs, leading to increased pulmonary vascular permeability and exacerbation of ALI. Mechanistically, lactate increased the lactylation of histone H3 at K18 (H3K18la), which promoted ACSL4 transcription in MPMVECs, resulting in excessive lipid peroxidation. Additionally, elevated H3K18la promoted LC3 transcription and indirectly upregulated NCOA4 expression through the transcription factor GATA2, facilitating ferritinophagy. Serum lactate levels were significantly correlated with ferroptosis levels in S-ARDS patients, and both were associated with poor patient prognosis. Conclusion: This study revealed a critical role for high lactate-derived histone lactylation in PMVEC ferroptosis and the progression of ALI during sepsis, providing new insights and potential therapeutic mechanisms.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"38 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPARs Mediated Diabetic Wound Healing Regulates Endothelial Cells Mitochondrial Function via Sonic Hedgehog Signaling","authors":"Shunli Rui, Fugang Xiao, Qin Li, Mengling Yang, Linrui Dai, Shiyan Yu, Xiaoshi Zhang, Xiaoyan Jiang, Seungkuk Ahn, Wenxin Wang, David G Armstrong, Hongyan Wang, Guangbin Huang, Wuquan Deng","doi":"10.1093/burnst/tkaf063","DOIUrl":"https://doi.org/10.1093/burnst/tkaf063","url":null,"abstract":"Background Diabetic foot ulcer (DFU) is a common and debilitating complication of diabetes, often leading to delayed wound healing. The peroxisome proliferator-activated receptors (PPARs) play a crucial role in regulating cellular metabolism and promoting angiogenesis. However, the mechanisms by which PPARs activation enhances wound healing, particularly in diabetic conditions, remain insufficiently understood. Methods Differentially expressed genes in DFU wounds and normal skin tissues were identified using the GEO database. PPARs expression in DFU neovascularization was validated by qRT-PCR, immunofluorescence, and western blotting. In vivo, diabetic mice treated with PPARs agonists (Chiglitazar) underwent wound healing assessment, including collagen deposition and angiogenesis. In vitro, high-glucose-induced endothelial cell models were used to evaluate PPARs activation effects on cell migration, tube formation, and mitochondrial function. Whole transcriptome sequencing and mitochondrial analysis were performed to explore the underlying mechanisms, particularly the sonic hedgehog (SHH) -mitochondrial axis. Results PPARs expression was significantly downregulated in DFU tissues (p < 0.05), and PPARs activation in diabetic mice enhanced wound healing, collagen deposition, granulation tissue proliferation, and angiogenesis (p < 0.05). In vitro, PPAR activation protected endothelial cells, promoting VEGF-A and CD31 expression, reducing apoptosis, and enhancing cell migration and tube formation (p < 0.05). Mechanistically, PPARs activated mitochondrial oxidative phosphorylation (OXPHOS) and membrane function through the SHH signaling pathway. SHH gene silencing reversed the effects of PPARs activation on mitochondrial function and angiogenesis. Conclusions PPARs signaling plays a critical role in DFU healing, with its inhibition linked to vascular dysfunction. Activation of the PPARs/SHH -mitochondrial axis significantly enhances endothelial cell metabolism and angiogenesis. This study provides insights into the molecular mechanisms of diabetic wound healing and supports the clinical potential of PPARs agonists for DFU treatment.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"100 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145035259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rescuing Endothelial Barrier Dysfunction in Sepsis: miR-23b-3p Antagonizes SMAD3-Mediated EndoMT and Vascular Hyperpermeability","authors":"Luofeng Jiang, Wei Zhang, Heng He, Xirui Tong, Futing Shu, Jiezhi Lin, Lu Yang, Hongchao Huang, Wenzhang Liu, Tianyi Liu, Yingying Liu, Pengfei Luo, Yongjun Zheng, Zhaofan Xia","doi":"10.1093/burnst/tkaf062","DOIUrl":"https://doi.org/10.1093/burnst/tkaf062","url":null,"abstract":"Background Sepsis-associated acute lung injury (ALI) is driven by endothelial barrier dysfunction and endothelial–mesenchymal transition (EndoMT), mediated by TGF-β1/SMAD3 signaling. Despite the therapeutic potential of SMAD3, current inhibitors face limitations. As endogenous small molecules that are closely related to physiological regulatory processes, miRNAs have more potential research value for regulating SMAD3. Methods Screening multiple databases revealed that miR-23b-3p was the sole miRNA targeting SMAD3. LPS-stimulated HUVECs and cecal ligation/puncture (CLP) mice were used to model sepsis. Lentivirus was used to construct stable strains. The functional performance and mechanism were verified by key techniques, including dual-luciferase assays, rescue experiments, RT–qPCR/Western blotting, monocyte adhesion/permeability assays, and histopathology. Results In LPS-stimulated HUVECs, miR-23b-3p downregulation correlated with TGF-β1/SMAD3 activation, EndoMT progression, and barrier disruption. miR-23b-3p overexpression reversed these effects by restoring the expression of junctional proteins and suppressing the expression of mesenchymal markers. ChIRP-qPCR, RNA-pull-down, and dual-luciferase assays confirmed the direct miR-23b-3p—SMAD3 3’UTR interaction. Rescue experiments demonstrated that miR-23b-3p counteracts TGF-β1/SMAD3 hyperactivation. In CLP mice, intratracheal agomiR-23b-3p attenuated lung injury, normalized alveolar architecture, and reduced vascular leakage by suppressing endothelial Smad3 upregulation. Conclusion miR-23b-3p is a SMAD3-targeting regulator that inhibits EndoMT and repairs endothelial barrier integrity. Mechanistically, miR-23b-3p preserves endothelial homeostasis via SMAD3-dependent EndoMT inhibition. This study provides mechanistic insights and a miRNA-based therapeutic strategy for sepsis-induced ALI.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"25 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145017556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A miRNA cocktail orchestrates coordinated cellular responses to promote diabetic wound healing","authors":"Yejing Huang, Liping Zhu, Jiating Wang, Ling Pan, Yong Yang, Dongqing Li","doi":"10.1093/burnst/tkaf060","DOIUrl":"https://doi.org/10.1093/burnst/tkaf060","url":null,"abstract":"Background Chronic wounds, particularly diabetic ulcers, impose significant health and economic burdens globally because of their complex pathology and the limited availability of therapeutic approaches. Multiple microRNAs (miRNAs) play crucial roles in regulating biological processes in wound healing. However, single-miRNA therapies may not fully overcome multifaceted barriers of impaired wound repair. Efforts to discover more effective wound therapies continue unabated. Methods In this study, we developed a microRNA cocktail that targets multiple critical phases of the wound healing: inflammation, re-epithelialization, granulation tissue formation and angiogenesis. This therapeutic cocktail includes locked nucleic acid (LNA)-modified mimics of miR-19b-3p, miR-132-3p, and miR-31-5p, along with an inhibitor of miR-92a-3p, which are delivered via in vivo-jetPEI as the carrier, addressing the multifaceted nature of wound repair mechanisms. The wound healing efficacy of the cocktail were systematically evaluated in mouse models of acute and chronic wounds. Results Local application of the miRNA cocktail to wounds markedly enhanced acute wound healing in wild-type mice, outperforming the effects of the individual miRNAs. Moreover, the miRNA cocktail accelerated diabetic wound healing by orchestrating coordinated cellular responses at the wound site and significantly decreasing inflammatory cytokine expression and CD68+ macrophage migration while promoting re-epithelialization, angiogenesis and granulation tissue formation. Notably, the cocktail also facilitated nerve regeneration in the wound area at day 30 post-injury. Conclusions Our findings suggest that this miRNA cocktail has potential therapeutic value for revitalizing the healing process in chronic wounds. Therefore, further investigations in controlled clinical trials are warranted to confirm the efficacy and applicability of this miRNA cocktail in a clinical setting.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"10 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Urine-Derived Stem Cells Rescue Cutaneous Manifestation and Suppress Inflammation and Fibrosis In Vitro and in a Mouse Model of Recessive Dystrophic Epidermolysis Bullosa","authors":"Xingli Zhou, Jie Tan, Yuting Song, Pengcheng Liu, Xiwen Zhang, Xun Feng, Yue Xiao, Yiyi Wang, Guoqing Liu, Wenqian Zhang, Qingyi Zhang, Yanlin Jiang, Yuan Liu, Longmei Zhao, Huiqi Xie, Wei Li","doi":"10.1093/burnst/tkaf058","DOIUrl":"https://doi.org/10.1093/burnst/tkaf058","url":null,"abstract":"Background Recessive dystrophic epidermolysis bullosa (RDEB) is a life-threatening disease characterized with persistent wound inflammation, tissue fibrosis, and even tumorigenesis in later stages. Despite its significant impact on patient health worldwide, treatment of RDEB has limited options. There in a clear need for now interventions. The goal of this study was to explore the potential efficacy of urine-derived stem cells (USCs) in RDEB. Methods We isolated human USCs from healthy donors, and assessed their therapeutic effects on RDEB both in vitro with tissue engineered skin in a three-dimensional co-culture system and in vivo with COL7A1−/− (RDEB) mice. Results USCs showed suppressive effects on expression of inflammation- and fibrosis- related genes involved in RDEB in vitro and in vivo. USCs could also extend the median life span (from 3 to 5 days), improve the expression of C7, and migrate to various organs of RDEB mice after intrahepatic administration. Conclusions In summary, these results suggest the potential effects of USCs on improving the the expression of C7 and would repair of RDEB, which supported the future use of USCs for the treatment of RDEB patients.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"1 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mechanism by which FGF23/FGFR-1 activates NOX2-ROS in vascular endothelial cells in the context of severe heat stroke-induced acute lung injury.","authors":"Zhengtao Gu, Jiazhuo Liu, Jiahui Fu, Yin Lu, Qin Li, Zhimin Zou, Jian Liu, Zhimin Zuo, Lei Su, Hongping Tan, Li Li","doi":"10.1093/burnst/tkae050","DOIUrl":"10.1093/burnst/tkae050","url":null,"abstract":"<p><strong>Background: </strong>The high mortality rate of severe heat stroke is mainly related to multiple organ dysfunction syndrome (MODS), and respiratory failure caused by acute lung injury (ALI) is a significant factor in the development of MODS during the course of severe heat stroke. Previous research has demonstrated that severe heat stroke-induced acute lung injury (sHS-ALI) is associated with an increase in reactive oxygen species (ROS) in vascular endothelial cells (VECs), but the specific initiating factors and intermediate mechanisms involved are unclear.</p><p><strong>Methods: </strong>In this study, the mRNA profiles of mouse lung tissues were analysed using high-throughput sequencing. Genome-wide knockout was performed using CRISPR-Cas9 technology to identify a cohort of differentially expressed genes that promote human umbilical vein endothelial cells survival after heat stress. The expression of key proteins [fibroblast growth factor 23 (FGF23), phosphorylated fibroblast growth factor receptor-1 (p-FGFR-1), FGFR-1, phosphorylated phospholipase C-γ2 (p-PLC-γ2), PLC-γ2, p-p47^phox, p67^phox, p22^phox, p40^phox, and nicotinamide adenine dinucleotide phosphate oxidase isoform 2 (NOX2)] involved in the FGF23/FGFR-1 mechanism was examined using western blotting and immunohistochemistry.</p><p><strong>Results: </strong>In this study, we first screened sHS-ALI target genes by cross-comparison <i>in vivo</i> and <i>in vitro</i> and found that FGF23 is the upstream promoter of sHS-ALI. Subsequent investigations involving the interference or inhibition of FGF23 expression revealed that FGF23 induced FGFR-1 Y766 phosphorylation during heat stress-induced VECs damage. In addition, FGF23 participated in NOX2 activation and ROS accumulation and was involved in the process of sHS-ALI. These findings indicated that the FGFR-1 Y766 site mutation strongly suppressed the production of p-PLC-γ2 and heat stress-induced NOX2-ROS activation in VECs. More importantly, mutation of the FGFR-1 Y766 phosphorylation site had no effect on FGF23 expression, and it was impossible to significantly induce the expression of p-PLC-γ2. Moreover, NOX2-ROS activation was inhibited, even in the presence of heat stress, the recombinant FGF23 protein, or combined stimulation.</p><p><strong>Conclusions: </strong>This study confirmed that FGF23/FGFR1 signalling, as an upstream priming factor, mediated NOX2-ROS activation in VECs after heat stress, thus participating in the sHS-ALI process. FGFR-1 Y766 phosphorylation is essential for FGF23/FGFR-1 signalling activation in VECs, which is involved in sHS-ALI. These findings further clarify the mechanism underlying sHS-ALI and contribute to reducing the mortality and morbidity of severe heat stroke.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"13 ","pages":"tkae050"},"PeriodicalIF":9.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12356372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metal Semiconductor Materials in Bone Diseases: Properties, Applications, and Future Perspectives","authors":"Wenshuang Sun, Yizhang Wu, Jia Sha, Xueru Song, Ziying Sun, Xi Cheng, Tao Yuan, Hong Qian, Xiaojiang Yang, Zhao Tang, Yueying Chen, Xinrui Sun, Liang Wang, Jia Meng, Zhongyang Lv, Nirong Bao","doi":"10.1093/burnst/tkaf055","DOIUrl":"https://doi.org/10.1093/burnst/tkaf055","url":null,"abstract":"The objective of bone tissue engineering is to develop innovative biomaterials and stimulation strategies to promote bone regeneration. Bioelectric materials play a crucial role in this domain owing to their inspiration of the inherent piezoelectric properties of bone. This review explores the progress made in utilizing metal semiconductor materials for bone tissue engineering, focusing on their operating mechanisms, various material classifications, and the ways they foster bone regeneration. First, the working principles of metal semiconductor materials are discussed, with an emphasis on the importance of bioelectric phenomena in regulating cell behavior. Owing to their roles in mimicking the electrophysiological microenvironment to promote bone regeneration, we highlight various types of metal semiconductor materials, such as metallic semiconductor materials, piezoelectric materials, and conductive biomaterials. Personalized and specific materials, including conductive smart scaffolds, modified implant surfaces, and those that target bone tissues, promote osseointegration, and exert antibacterial properties, serving diverse applications in bone tissue engineering. Additionally, to improve implant biocompatibility and osseointegration, the use of metal semiconductor materials in the design of orthopedic implants has shown promising clinical application prospects. Finally, looking forward to the future applications of metal semiconductor materials in bone engineering, integrating multiple functions, personalized medicine, and biodegradable materials, as well as the application of nanotechnology and 3D printing techniques, may arise to satisfy clinical requirements. This review also presents the biological characteristics of metal semiconductor materials and their recent applications in treating bone diseases, while also discussing innovative concepts for their design and development.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"40 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing injectable hydrogels for wound treatment: targeted control of oxidative stress toward personalized regeneration.","authors":"Thai Thanh T Hoang, Cuong Hung Luu, Joo Hee Kim, J Kent Leach, Ki Dong Park","doi":"10.1093/burnst/tkaf051","DOIUrl":"10.1093/burnst/tkaf051","url":null,"abstract":"<p><p>Wound injuries, including severe burns, diabetic foot ulcers, and chronic skin defects, remain a significant clinical burden due to their complexity, susceptibility to infection, and impaired healing, particularly in elderly individuals and patients with diabetes or vascular diseases. In these conditions, the wound healing process is disrupted by excessive oxidative stress, persistent inflammation, and microbial infection, ultimately leading to impaired tissue regeneration. These challenges highlight the urgent need for advanced wound care strategies capable of actively modulating the wound microenvironment to facilitate effective and timely healing. Among various hydrogel systems, injectable horseradish peroxidase (HRP)-catalyzed hydrogels have gained attention due to their biocompatibility, ease of application, tunable properties, ability to fill irregular wound geometries, versatility in material selection, and mild crosslinking conditions. These features make them promising candidates for multifunctional wound dressings in both acute and chronic wound management. This review provides a comprehensive overview of recent advancements in the development of injectable HRP-catalyzed hydrogels for wound treatment. We highlight key design strategies that confer multifunctional therapeutic capabilities, including hemostatic function, antibacterial activity, and reactive oxygen species-releasing and scavenging properties. Particular emphasis is placed on the incorporation of gasotransmitter-releasing components to regulate the wound microenvironment effectively. Furthermore, we discuss emerging strategies aimed at transforming these hydrogels into smart wound dressings with advanced functionalities, such as oxygen-releasing ability, electrical conductivity, and microbiome-modulating features. Finally, we emphasize the importance of developing scalable, safe, and personalized hydrogel systems capable of addressing the complex pathophysiology of chronic wounds and improving patient-specific wound care outcomes.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"13 ","pages":"tkaf051"},"PeriodicalIF":9.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12449077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Glucose Metabolism in Wound Healing: an overview","authors":"Tao Zhang, Youjing Yang, Junyu Jiang, Wenyu Du, Guangbin Huang, Dingyuan Du, Shasha Tao","doi":"10.1093/burnst/tkaf053","DOIUrl":"https://doi.org/10.1093/burnst/tkaf053","url":null,"abstract":"Glucose metabolism is the core process by which cells obtain energy, providing adenosine triphosphate (ATP) and metabolic intermediates through glycolysis and the tricarboxylic acid (TCA) cycle and supporting cell proliferation, migration, and functional maintenance. It not only fuels cells but also cranks out nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. This NADPH is crucial for fending off oxidative stress, keeping immune responses in check, and playing a role in cell signaling. During the process of wound healing, glucose metabolism plays a crucial role in each stage. In the early stage, cells rely on glycolysis to generate energy for proliferation and migration; during the inflammatory phase, immune cells generate reactive oxygen species through glucose metabolism to eliminate pathogens; and during the proliferation and remodeling phase, glucose metabolism supports the generation of the extracellular matrix and tissue repair. However, in chronic wounds, abnormal glucose metabolism increases oxidative stress and inflammatory responses, significantly delaying wound healing. Understanding how abnormal glucose metabolism affects the wound microenvironment and cell function can help researchers develop new therapeutic strategies. Therefore, this review breaks down how glucose metabolism works at each stage of wound healing. We're highlighting its potential as something we can target therapeutically, and hoping to spark some fresh ideas and avenues for research and clinical use down the road.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"143 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}