Burns & Trauma最新文献

{"title":"Breaking the vicious cycle of impaired angiogenesis and chronic inflammation in diabetic wounds: a bioengineered microneedle system delivering RGD-modified M2 exosomes.","authors":"HongYu Wang, BaoHua Wei, BaiShi Wang, Mi Chai, Jing Ren, Yan Han, LingLi Guo","doi":"10.1093/burnst/tkag013","DOIUrl":"10.1093/burnst/tkag013","url":null,"abstract":"<p><strong>Background: </strong>Persistent local tissue hypoperfusion and chronic inflammation are central challenges in diabetic wound management. The development of effective therapeutic strategies to mitigate prolonged inflammation and enhance tissue vascularization is crucial for accelerating diabetic wound healing. This study aimed to develop soluble microneedle materials that simultaneously target both aspects to improve the clinical prognosis of diabetic wounds.</p><p><strong>Methods: </strong>A stable macrophage cell line overexpressing basic fibroblast growth factor (bFGF) was established using lentiviral transfection. After M2 polarization was induced with interleukin-4 (IL-4) and IL-10, exosomes were isolated via ultracentrifugation and surface-functionalized with arginine-glycine-aspartic acid (RGD)-targeting peptides. The reparative effects of these exosomes on human umbilical vein endothelial cells (HUVECs) with high glucose-induced injury were evaluated using scratch test, 5-ethynyl-2'-deoxyuridine (EdU) staining, and cell counting kit-8 assays. A delivery system based on soluble hyaluronic acid microneedles (MNs) loaded with engineered exosomes was then developed. Its therapeutic efficacy was evaluated in a diabetic wound mouse model, and the underlying mechanisms were explored via ribonucleic acid (RNA) sequencing.</p><p><strong>Results: </strong>Targeted engineered exosomes (TE-Exos) derived from bFGF-overexpressing M2 macrophages with surface RGD modification were successfully prepared. Assays revealed that TE-Exos exhibited specific targeting to HUVECs with high glucose-induced injury and significantly enhanced cellular proliferation, migration, and tube formation. Furthermore, the polarization ratio of macrophages improved after TE-Exos treatment. <i>In vivo</i>, the MN-mediated delivery of TE-Exos markedly accelerated diabetic wound healing by enhancing re-epithelialization, collagen deposition, and angiogenesis. Furthermore, the treatment modulated the wound microenvironment by reducing the infiltration of proinflammatory M1 macrophages while increasing the proportion of reparative M2 macrophages. RNA sequencing analysis indicated that the therapeutic effects were mediated primarily through the inhibition of excessive inflammation and the activation of angiogenesis-related signaling pathways.</p><p><strong>Conclusions: </strong>This innovative strategy breaks the vicious cycle of impaired angiogenesis and chronic inflammation in diabetic wounds through a synergistic mechanism involving 'angiogenesis, inflammation regulation, and precise delivery'. The combination of targeted exosome engineering with an MN delivery system not only overcomes the limitations of conventional growth factor therapies but also enables intelligent modulation of the wound microenvironment, offering novel theoretical insights and practical approaches for clinical translation.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag013"},"PeriodicalIF":11.0,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13340465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403776","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":"Melatonin promotes skin flap survival by inhibiting ferroptosis","authors":"Mi Liu, Jiacheng Hu, Jiayi Huang, Zhefeng Cai, Peng Zou, Jing Bu, Shanshan Yu, Yuxi Zhou, Xiaoqiong Jiang, Lianfang Gan, Shuhong Tian, Lei Dong, Fenzan Wu, Huiming Deng, Jian Xiao","doi":"10.1093/burnst/tkag012","DOIUrl":"https://doi.org/10.1093/burnst/tkag012","url":null,"abstract":"Background Random skin flaps application is considerably limited by postoperative complications, particularly distal tissue ischemia and necrosis. Melatonin, a molecule with well-documented antioxidant and cytoprotective properties, has shown promise in protecting ischemic tissues. However, its specific role in regulating ferroptosis during ischemic flap injury, as well as its safety and efficacy in primate models (a key step for clinical translation), remains to be systematically validated. In this study, we aimed to promote angiogenesis within flap tissue through exogenous melatonin administration, and to inhibit ferroptosis to mitigate ischemia-reperfusion injury, presenting a novel strategy for enhancing flap survival rates. Methods A random skin flap was constructed in C57BL/6J mice. After melatonin treatment for seven days, the influence of melatonin on the levels of oxidative stress, iron accumulation, and mitochondrial morphology within the skin flap tissue were assessed. We used Transwell migration assays, tube formation assays, flow cytometry and immunofluorescence staining to determine the effects of melatonin in vitro. The ferroptosis inducer erastin was used in combination with melatonin to treat random skin flap mice and Tert-butyl hydroperoxide (TBHP) induced cellular models, And the pathway through which melatonin counteracts iron mutations was explored. Lastly, we conducted experiments using nonhuman primate (NHP) models and analyzed the protective effects of melatonin on ischemic flaps in macaques, highlighting its potential for clinical translation. Results Melatonin ameliorated the survival area of ischemic flaps in mice, enhanced angiogenesis, reduced mitochondrial damage, and also suppressed lipid peroxidation and iron ion accumulation. Melatonin attenuated TBPH-induced cell death, lipid peroxidation, and mitochondrial damage in vitro. Further mechanistic studies revealed that melatonin inhibited ferroptosis, accompanied by nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), and increases the expression of downstream gene (effector) heme oxygenase-1 (HO-1). More importantly, experiments in macaques demonstrated that melatonin could enhance flap viability and angiogenesis, and exhibited good safety profile. Conclusion Melatonin enhanced flap viability in mice and macaques by inhibiting ferroptosis, boosting angiogenesis, and attenuating oxidative stress injury.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"41 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101432","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":"Targeting mitofusin 1-mediated mitochondrial dynamics to suppress neuroinflammation and pyroptosis after traumatic brain injury.","authors":"Tao Liu, Liang Mi, Bo Chen, Meng Nie, Shuo Wang, Bo Wang, Yunhu Yu, Rongcai Jiang","doi":"10.1093/burnst/tkag011","DOIUrl":"10.1093/burnst/tkag011","url":null,"abstract":"<p><strong>Background: </strong>Traumatic brain injury (TBI) can cause neuroinflammation and neuronal death. The role of mitochondrial dysfunction in regulating inflammasome activation during TBI remains unclear. This study aims to explore mitochondrial regulation of neuroinflammation and pyroptosis after TBI.</p><p><strong>Methods: </strong>We used a mouse TBI model and <i>in vitro</i> scratch-injured HT22 cells and primary neurons to examine changes in mitochondrial dynamics and nucleotide-binding oligomerization domain-like receptors family pyrin domain-containing 3 (NLRP3) inflammasome activation. Metformin treatment, mitofusin 1 (Mfn1) knockdown and regulation of the Mfn1 pathway were applied to evaluate the therapeutic effects and mechanisms.</p><p><strong>Results: </strong>TBI triggered NLRP3 inflammasome activation and neuronal pyroptosis, along with impaired mitochondrial function and oxidative stress. Metformin reduced inflammasome activation, improved mitochondrial homeostasis, and alleviated neuronal injury. These effects were lost when Mfn1 was silenced, highlighting its essential role. Furthermore, we determined that the AMPK pathway modulates these observed effects.</p><p><strong>Conclusion: </strong>Metformin protects against TBI-induced neuronal damage by restoring Mfn1-dependent mitochondrial dynamics and suppressing inflammasome activation. Mfn1 is a key mediator linking mitochondrial health to neuroinflammatory responses in TBI.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag011"},"PeriodicalIF":11.0,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866965","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":"A novel method for targeting lymphatic vessel imaging: methylene blue nanoparticle integrated with dissolvable microneedles","authors":"Chengyao Han, Beibei Wu, Chunxiao Cui, Peiru Min, Xinxian Meng, Yuhao Sun, Ke Wen, Chuanliang Feng, Yixin Zhang, Xueqian Wang, Ke Li","doi":"10.1093/burnst/tkaf067","DOIUrl":"https://doi.org/10.1093/burnst/tkaf067","url":null,"abstract":"The lymphatic system serves many more functions than simply in maintaining tissue fluid homeostasis, and its structural and functional changes indicate the occurrence of disease. Current clinical methods for the assessment of the lymphatic system, however, are severely limited because of their nontargeting ability, invasiveness, high cost, and radiation risk. Herein, we propose a simple and painless method for visualizing and quantifying the lymphatic system. This method is based on the noninvasive administration of a novel lymphatic tracer via dissolvable microneedles (MNs), followed by the application of a portable detection device for near-infrared (NIR) imaging. The tracer is prepared by incorporating the clinically approved NIR fluorescent dye methylene blue (ME) into nanomaterials (MPEG-PCL@ME). This novel tracer displays superior fluorescence properties, stability, biocompatibility, and targeting features in comparison with ME solution alone. Lymphography with MPEG-PCL@ME in vivo clearly revealed the lymphatic vessel morphology. Notably, compared with ME and ICG, MPEG-PCL@ME can easily identify the dominant lymphatic vessels and nodes in rats with higher imaging quality. Furthermore, a series of segmental contracting sections are detected with MPEG-PCL@ME, allowing straightforward identification of the lymphatic pump, which provides direct evidence for exquisitely evaluating lymphatic functions.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"38 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056085","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":"Multifunctional nanofibrous membranes enhance diabetic wound healing by inhibiting endothelial pyroptosis and regulating macrophage polarization.","authors":"Shuang Deng, Ting Ying, Xu Zhang, Farnaz Ghorbani, Wen Luo, Chengqing Yi, Dejian Li","doi":"10.1093/burnst/tkag005","DOIUrl":"10.1093/burnst/tkag005","url":null,"abstract":"<p><strong>Background: </strong>Persistent oxidative stress and aberrant inflammatory responses are major contributors to delayed wound healing in diabetic patients. Endothelial cell pyroptosis, a form of inflammatory programmed cell death, plays a critical role in vascular dysfunction and impaired tissue regeneration in diabetic wounds. Targeting endothelial pyroptosis therefore represents a promising therapeutic strategy. This study aims to develop a multifunctional nanofibrous scaffold capable of suppressing oxidative stress-induced endothelial pyroptosis while modulating the inflammatory microenvironment to promote angiogenesis and diabetic wound repair.</p><p><strong>Methods: </strong>In this study, a pH-responsive nanoplatform based on zinc-imidazolate metal-organic frameworks (ZIF-8) was constructed for the controlled delivery of luteolin (Lut), a natural flavonoid with anti-inflammatory and antioxidant properties. The physicochemical characteristics, drug-loading efficiency, and pH-responsive release behavior of Lut@ZIF-8 nanoparticles were systematically evaluated. The effects of Lut@ZIF-8 on oxidative stress, endothelial pyroptosis, and angiogenic function were investigated <i>in vitro</i>, while therapeutic efficacy was further assessed in a diabetic mouse wound model using Lut@ZIF-8-loaded fibrous scaffolds.</p><p><strong>Results: </strong>Lut@ZIF-8 nanoparticles exhibited uniform morphology, high drug-loading efficiency, and sustained drug release under mildly acidic conditions mimicking the diabetic wound microenvironment. <i>In vitro</i>, Lut@ZIF-8 effectively suppressed reactive oxygen species accumulation and inhibited endothelial cell pyroptosis by downregulating the activation of NLRP3 inflammasome components, including caspase-1 and GSDMD, thereby preserving endothelial barrier integrity and angiogenic capacity. <i>In vivo</i>, Lut@ZIF-8-loaded scaffolds significantly reduced inflammatory cytokine expression, enhanced collagen deposition, promoted neovascularization and re-epithelialization, and ultimately accelerated wound closure in diabetic mice.</p><p><strong>Conclusions: </strong>The pH-responsive Lut@ZIF-8 nanoplatform effectively modulates oxidative stress and endothelial cell pyroptosis in diabetic wounds, thereby promoting angiogenesis and tissue regeneration. This strategy provides a promising and innovative therapeutic approach for the treatment of chronic diabetic wounds.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag005"},"PeriodicalIF":11.0,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13011808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509320","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":"<i>Saccharomyces boulardii</i> in patients with severe acute pancreatitis: a single center, open-label randomized controlled trial.","authors":"Jia-Lin He, Lei Ran, Xu Xiao, Yu Su, Hui Lin, Cheng Lu, Bo Tang, Shiming Yang","doi":"10.1093/burnst/tkag006","DOIUrl":"10.1093/burnst/tkag006","url":null,"abstract":"<p><strong>Background: </strong>Nosocomial infections in patients with severe acute pancreatitis (SAP) are frequently driven by impaired intestinal barrier function, which facilitates bacterial translocation and contributes to adverse clinical outcomes. <i>Saccharomyces boulardii</i> (<i>S. boulardii</i>) can reconstitute gut microbiota composition. We investigated whether <i>S. boulardii</i> combined with enteral nutrition (EN) affects the microbiome and nosocomial infections in SAP.</p><p><strong>Methods: </strong>This study is a single centre, open-label randomized controlled trial. We included 50 patients with SAP in a Chinese gastroenterology intensive care unit (ICU), randomized to Probiotic group (<i>S. boulardii</i> and EN) or the Control group (EN). Throat/oropharyngeal and rectal swabs were collected from patients with SAP on days 0, 1, 3, 6, 9, 12, and 15 of ICU admission. The primary endpoints were nosocomial infection and fungemia, whereas the secondary endpoints were ICU mortality, 28-day mortality, ICU stay, and length of hospital stay. All samples were subjected to full-length 16 s rRNA and internal transcribed spacer (ITS) sequencing. Multivariate analysis was performed using normalized microbial and corresponding clinical data.</p><p><strong>Results: </strong>After data processing, 213 16S rRNA and 120 ITS samples were analysed. <i>S. boulardii</i> prevented nosocomial infections (0/27 in the Probiotic group <i>vs</i> 5/23 in the Control group; <i>P</i> < 0.05). Intestinal fungi were closely associated with nosocomial infections. Bioinformatic analysis showed that <i>S. boulardii</i> prevented nosocomial infections by reducing intestinal bacterial perturbation and inhibiting the proliferation of <i>Enterococcus</i> in the intestine, and <i>Candida</i> in the respiratory tract and intestines.</p><p><strong>Conclusions: </strong><i>S. boulardii</i> in patients with SAP may positively alter the respiratory and intestinal microbiome and decrease the incidence of nosocomial infections.</p><p><strong>Trial registration: </strong>This study was approved by the Ethics Committee of Xinqiao Hospital, Army Medical University, Chongqing China (2021-yd030-01), which was retrospectively registered at the Chinese Clinical Trial Registry (ChiCTR2200056011, Date of Registration: 30/01/2022 https://www.chictr.org.cn/showproj.html?proj=151215).</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 ","pages":"tkag006"},"PeriodicalIF":11.0,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12919443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269854","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":"RNA Modifications: Molecular Orchestrators of Wound Healing","authors":"Xiuying Guo, Lele Liu, Junqi Yang, Yuhe Dai, Qianbo Zhang, Rifang Gu, Min Tan, Ming Tang, Xuqiang Nie","doi":"10.1093/burnst/tkag010","DOIUrl":"https://doi.org/10.1093/burnst/tkag010","url":null,"abstract":"Wound healing is a highly coordinated biological process traditionally divided into three phases: Inflammatory, proliferative, and remodeling. Diabetes and acute trauma markedly disrupt these stages, resulting in delayed wound closure, persistent inflammation, and impaired tissue regeneration. This review focuses on three trauma-relevant contexts: (i) Skin wounds, including diabetic ulcers and burns; (ii) bone fracture healing; (iii) corneal epithelial and stromal injury. Robust in vivo evidence is synthesized to delineate the mechanistic roles of the four principal RNA modifications: N6-methyladenosine, 5-methylcytosine, N7-methylguanosine, and N4-acetylcytidine. Additionally, the roles of RNA modification writers, erasers, and readers in regulating macrophage polarization, stem and progenitor cell fate, angiogenesis, lymphangiogenesis, and extracellular matrix remodeling are examined. Evidence across different tissues and wound healing phases is integrated rather than presented descriptively. Methodological limitations are highlighted, and knowledge gaps are identified alongside testable hypotheses. Translational opportunities with direct relevance to burn and trauma management are emphasized. This review aims to integrate mechanistic and translational insights into a coherent framework for therapeutic intervention. By defining how RNA modifications intersect with distinct wound healing phases, concrete therapeutic entry points and delivery strategies relevant to burns and trauma are identified, including topical hydrogels, exosome-based therapies, and bone-targeted nanoparticles. Designs for pragmatic clinical trials and biomarker strategies that enable translation of preclinical findings to patients are also discussed.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"50 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972469","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":"Modulating Hypertrophic Scar Formation by Targeting Endothelial TRPV1/NF-κB/IL-6 Axis to Regulate Angiogenesis","authors":"Hao Ma, Liuhanghang Cheng, Ruoyu Ling, Jingyi Chen, Shunuo Zhang, Shujing Lin, Liang Ding, Chengliang Deng, Yixin Zhang, Peiru Min","doi":"10.1093/burnst/tkag009","DOIUrl":"https://doi.org/10.1093/burnst/tkag009","url":null,"abstract":"Background Noxious lifestyle factors including spicy diets and hot baths may lead to scar formation and recurrence. These phenomena are related to the activation of the transient receptor potential vanilloid (TRPV1) cation channel. Our previous study revealed significant upregulation of TRPV1 expression in the dermis of hypertrophic scar (HS), while the exact underlying mechanism of TRPV1 activation in HS remains ill-defined. Methods Firstly, this study employs single-cell RNA sequencing technology to analyze the association between vascular endothelial cells and the development of HS. Complementarily, bioinformatics analysis combined with histological validation is utilized to investigate the relationship between TRPV1 channels and aberrant angiogenesis within HS formation. Furthermore, the correlation between TRPV1 activation and HS phenotypes is rigorously validated at the in vivo level. In parallel, in vitro experiments are conducted to elucidate the impact of TRPV1 channel activation on the biological behaviors and functions of vascular endothelial cells. Subsequently, key downstream signaling pathways of TRPV1 are screened, and their molecular mechanisms in regulating vascular endothelial cell-mediated angiogenesis are systematically verified. Finally, a comprehensive analysis is performed to establish the clinical relevance of the TRPV1/nuclear factor kappa-B (NF-κB)/interleukin-6 (IL-6) axis with vascularization severity and adverse prognostic outcomes in hypertrophic scarring. Results Single-cell RNA sequencing revealed significant cellular heterogeneity in vascular endothelial cells between normal skin (NS) and HS, indicating activated angiogenesis and substantial vascular endothelial cell alterations during HS development. Bulk RNA-seq and clinical analyses further confirmed this angiogenesis activation, demonstrating a close association with TRPV1 channel activation. In vivo studies established that capsaicin (CAP)-induced TRPV1 activation exacerbated HS progression through enhanced angiogenesis, whereas TRPV1 ablation or local inhibition markedly attenuated this effect. In vitro experiments demonstrated TRPV1 activation regulated angiogenesis by promoting pro-angiogenic phenotypes. Transcriptomic analysis and functional validation identified the IL-6/Signal Transducer and Activator of Transcription 3 (STAT3) pathway as a downstream NF-κB-dependent pro-angiogenic axis mediated by TRPV1 in HS vascular endothelial cells. Critically, dermal overexpression of the TRPV1/NF-κB/IL-6 axis in HS patients correlated strongly with both disease severity and recurrence. Conclusions Here, we show that the development of HS is strongly correlated with endothelial angiogenic activity. TRPV1 activation by CAP enhances proangiogenic processes including endothelial proliferation, migration and tubule formation, while reducing apoptosis through the TRPV1/ NF-κB/ IL-6 axis. In a rabbit ear HS model, stimulation of TRPV1 contributes to the formation of HS ","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"19 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986323","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":"Mitochondrial Dynamics in Skin Health and Disease: Energy, Ageing, and Therapeutic Perspectives","authors":"Rong Zhang, Tianhao Li, Fengzhou Du, Jiuzuo Huang, Nanze Yu, Xiao Long","doi":"10.1093/burnst/tkag008","DOIUrl":"https://doi.org/10.1093/burnst/tkag008","url":null,"abstract":"As cellular energy metabolic hubs, mitochondria undergo dynamic fusion–fission cycles and autophagy that enable rapid adaptation to cellular energy demands and stress conditions. In addition to their role in energy metabolism, mitochondria are integral to cellular homeostasis and regulate cell cycle progression, differentiation, and apoptosis pathways. In recent years, the importance of mitochondrial function in skin health and disease has garnered increasing attention. Mitochondrial dysfunction has been implicated in a spectrum of skin disorders, including skin ageing, psoriasis, vitiligo, keloids, scleroderma, and skin cancer. The pathogenesis of these conditions is closely linked to mitochondrial DNA (mtDNA) damage, excessive reactive oxygen species (ROS) production, and alterations in mitochondrial metabolic pathways. In terms of therapeutic strategies, this review summarizes a range of mitochondrion-targeted interventions. These treatments include the activation of the PGC-1α pathway to increase mitochondrial ATP synthesis, the use of antioxidants to mitigate mitochondrial ROS production, and the application of bioactive compounds and drugs to protect mitochondria or promote mtDNA repair. These approaches not only contribute to improved skin health but also provide novel insights for the treatment of skin diseases. Additionally, mitochondrial transplantation technology has shown considerable promise in skin regeneration and wound healing and is emerging as a new frontier for skin tissue repair.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"14 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961705","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":"Hybrid Nanovesicles Promote Diabetic Wound Healing via Dual-Targeted Multimodal Therapy","authors":"Zhichao Ruan, Yi Zheng, Guoyong Jiang, Jing Chen, Jiahe Guo, Chengqi Yan, Dong Liu, Shuoyuan Liu, Yufeng Wang, Pengjuan Nie, Diandian Li, Zijie Chen, Jia Tian, Zhenbing Chen, Xiaofan Yang","doi":"10.1093/burnst/tkag004","DOIUrl":"https://doi.org/10.1093/burnst/tkag004","url":null,"abstract":"Background Diabetic wounds remain difficult to treat due to persistent oxidative stress, chronic inflammation, and vascular dysfunction. These factors reinforce each other, forming a vicious cycle that leads to delayed healing, poor angiogenesis, and high amputation risk. Existing therapies often fail because they are unable to address these challenges simultaneously. Therefore, this study aimed to develop a hybrid extracellular vesicle system that targets these multiple barriers concurrently to promote diabetic wound healing. Methods A biohybrid nanovesicle system (DFO@HEVs) was built by fusing endothelial cell-derived extracellular vesicles with neutrophil-derived nanovesicles (forming hybrid extracellular vesicles, HEVs), which were loaded with deferoxamine (DFO). The vesicles were tested for their physicochemical properties, drug loading, and safety. Therapeutic effects were studied in vitro using HG/PA-stimulated endothelial cells and macrophages and in vivo in diabetic mouse wounds. The analyses included microscopy, flow cytometry, histology, transcriptomics, and database-based single-cell RNA sequencing. Results DFO@HEVs showed dual targeting: homing to endothelial cells via CXCR4 and to inflamed sites via β2 integrin. They enhanced endothelial uptake, promoted angiogenesis through PI3K/AKT/HIF-1α and VEGF signaling pathways, and reduced oxidative stress and ferroptosis by activating Nrf2 and upregulating antioxidant genes. They also shifted macrophages toward an anti-inflammatory M2 phenotype, boosted efferocytosis, and suppressed NF-κB/NLRP3-driven inflammation. In diabetic mice, treatment with DFO@HEVs accelerated wound closure, re-epithelialization, collagen deposition, and new vessel formation, while lowering neutrophil infiltration, ROS levels, ferroptosis, and pro-inflammatory cytokines, creating a healing-supportive environment. Conclusions DFO@HEVs provided a hybrid nanovesicle system for combined membrane and drug delivery. By promoting angiogenesis, limiting ferroptosis, and resolving inflammation, they disrupted the cycle that prevented diabetic wound repair. This approach shows a strong potential as a new treatment for chronic wounds.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"120 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961704","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}