Bacterial infections pose a serious threat to human health. While antibiotics have been effective in treating bacterial infectious diseases, antibiotic resistance significantly reduces their effectiveness. Therefore, it is crucial to develop new and effective antimicrobial strategies. Metal–organic frameworks (MOFs) have become ideal nanomaterials for various antimicrobial applications due to their crystalline porous structure, tunable size, good mechanical stability, large surface area, and chemical stability. Importantly, the performance of MOFs can be adjusted by changing the synthesis steps and conditions. Pure MOFs can release metal ions to modulate cellular behaviors and kill various microorganisms. Additionally, MOFs can act as carriers for delivering antimicrobial agents in a desired manner. Importantly, the performance of MOFs can be adjusted by changing the synthesis steps and conditions. Furthermore, certain types of MOFs can be combined with traditional photothermal or other physical stimuli to achieve broad-spectrum antimicrobial activity. Recently an increasing number of researchers have conducted many studies on applying various MOFs for diseases caused by bacterial infections. Based on this, we perform this study to report the current status of MOFs-based antimicrobial strategy. In addition, we also discussed some challenges that MOFs currently face in biomedical applications, such as biocompatibility and controlled release capabilities. Although these challenges currently limit their widespread use, we believe that with further research and development, new MOFs with higher biocompatibility and targeting capabilities can provide diversified treatment strategies for various diseases caused by bacterial infections.
{"title":"Multifunctional metal–organic frameworks as promising nanomaterials for antimicrobial strategies","authors":"Qian-Jin Li, Fei Xing, Wen-Ting Wu, Man Zhe, Wen-Qian Zhang, Lu Qin, Li-Ping Huang, Long-Mei Zhao, Rui Wang, Ming-Hui Fan, Chen-Yu Zou, Wei-Qiang Duan, Jesse Li-Ling, Hui-Qi Xie","doi":"10.1093/burnst/tkaf008","DOIUrl":"https://doi.org/10.1093/burnst/tkaf008","url":null,"abstract":"Bacterial infections pose a serious threat to human health. While antibiotics have been effective in treating bacterial infectious diseases, antibiotic resistance significantly reduces their effectiveness. Therefore, it is crucial to develop new and effective antimicrobial strategies. Metal–organic frameworks (MOFs) have become ideal nanomaterials for various antimicrobial applications due to their crystalline porous structure, tunable size, good mechanical stability, large surface area, and chemical stability. Importantly, the performance of MOFs can be adjusted by changing the synthesis steps and conditions. Pure MOFs can release metal ions to modulate cellular behaviors and kill various microorganisms. Additionally, MOFs can act as carriers for delivering antimicrobial agents in a desired manner. Importantly, the performance of MOFs can be adjusted by changing the synthesis steps and conditions. Furthermore, certain types of MOFs can be combined with traditional photothermal or other physical stimuli to achieve broad-spectrum antimicrobial activity. Recently an increasing number of researchers have conducted many studies on applying various MOFs for diseases caused by bacterial infections. Based on this, we perform this study to report the current status of MOFs-based antimicrobial strategy. In addition, we also discussed some challenges that MOFs currently face in biomedical applications, such as biocompatibility and controlled release capabilities. Although these challenges currently limit their widespread use, we believe that with further research and development, new MOFs with higher biocompatibility and targeting capabilities can provide diversified treatment strategies for various diseases caused by bacterial infections.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"33 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031304","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}
Min Wang, Xinyu Zhao, Yuyu Cui, Hengshuo Gui, Shuai Wang, Zhuang Liu, Xianwen Wang
Burn injuries are associated with high morbidity and mortality, and severe burns trigger many pathophysiological reactions, such as metabolic changes, distributive shock, and inflammatory responses, which are potentially devastating to patients. Burn wound management necessitates infection prevention, anti-inflammation, pain management, and growth factor management, but significant obstacles remain. Extracellular vesicles (EVs) are lipid bilayer vesicles secreted by various cell types, including mammalian cells, plant cells, and even prokaryotes, They are widely involved in various biological processes, such as cell survival, neovascularization, and immunomodulation. EVs are abundant in components that can play a significant role in different stages of wound repair and at different subcellular levels simultaneously by transporting various active contents, such as proteins and nucleic acids. Moreover, EVs are detectable in many biofluids of burn injury patients and are thus regarded as novel biomarkers for monitoring therapeutic response and predicting prognosis. This review summarizes the biological roles of EVs and their mechanisms of action in burn injury are summarized. The prospects and opportunities for the clinical application of EVs in burn wounds are also discussed. This review will stimulate and guide additional in-depth studies of EVs in burn wound repair, provide a new therapy for burn wounds, and provide a reference and guidance for applying EVs in clinical wound repair.
{"title":"Extracellular vesicles in burn injury: roles, mechanisms, and applications","authors":"Min Wang, Xinyu Zhao, Yuyu Cui, Hengshuo Gui, Shuai Wang, Zhuang Liu, Xianwen Wang","doi":"10.1093/burnst/tkaf006","DOIUrl":"https://doi.org/10.1093/burnst/tkaf006","url":null,"abstract":"Burn injuries are associated with high morbidity and mortality, and severe burns trigger many pathophysiological reactions, such as metabolic changes, distributive shock, and inflammatory responses, which are potentially devastating to patients. Burn wound management necessitates infection prevention, anti-inflammation, pain management, and growth factor management, but significant obstacles remain. Extracellular vesicles (EVs) are lipid bilayer vesicles secreted by various cell types, including mammalian cells, plant cells, and even prokaryotes, They are widely involved in various biological processes, such as cell survival, neovascularization, and immunomodulation. EVs are abundant in components that can play a significant role in different stages of wound repair and at different subcellular levels simultaneously by transporting various active contents, such as proteins and nucleic acids. Moreover, EVs are detectable in many biofluids of burn injury patients and are thus regarded as novel biomarkers for monitoring therapeutic response and predicting prognosis. This review summarizes the biological roles of EVs and their mechanisms of action in burn injury are summarized. The prospects and opportunities for the clinical application of EVs in burn wounds are also discussed. This review will stimulate and guide additional in-depth studies of EVs in burn wound repair, provide a new therapy for burn wounds, and provide a reference and guidance for applying EVs in clinical wound repair.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"25 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020691","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}
Background Neuronal structure is disrupted after spinal cord injury (SCI), causing functional impairment. The effectiveness of exercise therapy (ET) in clinical settings for nerve remodeling post-SCI and its underlying mechanisms remain unclear. This study aims to explore the effects and related mechanisms of ET on nerve remodeling in SCI rats. Methods We randomly assigned rats to various groups: sham-operated group, sham-operated + ET, SCI alone, SCI + H89, SCI + ET, and SCI + ET + H89. Techniques including motor-evoked potential (MEP), video capture and analysis, the Basso–Beattie–Bresnahan (BBB) scale, western blotting, transmission electron microscopy, hematoxylin and eosin staining, Nissl staining, glycine silver staining, immunofluorescence, and Golgi staining were utilized to assess signal conduction capabilities, neurological deficits, hindlimb performance, protein expression levels, neuron ultrastructure, and tissue morphology. H89—an inhibitor that targets the protein kinase A (PKA)/cAMP response element-binding (CREB) signaling pathway—was employed to investigate molecular mechanisms. Results This study found that ET can reduce neuronal damage in rats with SCI, protect residual tissue, promote the remodeling of motor neurons, neurofilaments, dendrites/axons, synapses, and myelin sheaths, reorganize neural circuits, and promote motor function recovery. In terms of mechanism, ET mainly works by mediating the PKA/CREB signaling pathway in neurons. Conclusions Our findings indicated that: (1) ET counteracted the H89-induced suppression of the PKA/CREB signaling pathway following SCI; (2) ET significantly alleviated neuronal injury and improved motor dysfunction; (3) ET facilitated neuronal regeneration by mediating the PKA/CREB signaling pathway; (4) ET enhanced synaptic and dendritic spine plasticity, as well as myelin sheath remodeling, post-SCI through the PKA/CREB signaling pathway.
{"title":"Exercise therapy facilitates neural remodeling and functional recovery post-spinal cord injury via PKA/CREB signaling pathway modulation in rats","authors":"Xinwang Ying, Qingfeng Xie, Yanfang Zhao, Jiamen Shen, Junqing Huang, Zhiyi Feng, Liuxi Chu, Junpeng Xu, Dawei Jiang, Ping Wu, Yanming Zuo, Shengcun Li, Chang Jiang, Xiaokun Li, Zhouguang Wang","doi":"10.1093/burnst/tkae058","DOIUrl":"https://doi.org/10.1093/burnst/tkae058","url":null,"abstract":"Background Neuronal structure is disrupted after spinal cord injury (SCI), causing functional impairment. The effectiveness of exercise therapy (ET) in clinical settings for nerve remodeling post-SCI and its underlying mechanisms remain unclear. This study aims to explore the effects and related mechanisms of ET on nerve remodeling in SCI rats. Methods We randomly assigned rats to various groups: sham-operated group, sham-operated + ET, SCI alone, SCI + H89, SCI + ET, and SCI + ET + H89. Techniques including motor-evoked potential (MEP), video capture and analysis, the Basso–Beattie–Bresnahan (BBB) scale, western blotting, transmission electron microscopy, hematoxylin and eosin staining, Nissl staining, glycine silver staining, immunofluorescence, and Golgi staining were utilized to assess signal conduction capabilities, neurological deficits, hindlimb performance, protein expression levels, neuron ultrastructure, and tissue morphology. H89—an inhibitor that targets the protein kinase A (PKA)/cAMP response element-binding (CREB) signaling pathway—was employed to investigate molecular mechanisms. Results This study found that ET can reduce neuronal damage in rats with SCI, protect residual tissue, promote the remodeling of motor neurons, neurofilaments, dendrites/axons, synapses, and myelin sheaths, reorganize neural circuits, and promote motor function recovery. In terms of mechanism, ET mainly works by mediating the PKA/CREB signaling pathway in neurons. Conclusions Our findings indicated that: (1) ET counteracted the H89-induced suppression of the PKA/CREB signaling pathway following SCI; (2) ET significantly alleviated neuronal injury and improved motor dysfunction; (3) ET facilitated neuronal regeneration by mediating the PKA/CREB signaling pathway; (4) ET enhanced synaptic and dendritic spine plasticity, as well as myelin sheath remodeling, post-SCI through the PKA/CREB signaling pathway.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"75 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020357","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}
Xingqian Wu, Rifang Gu, Ming Tang, Xingrui Mu, Wenjie He, Xuqiang Nie
Wound healing is a complex and multistep biological process that involves the cooperation of various cell types. Programmed cell death, including apoptosis and necrotizing apoptosis, plays a crucial role in this process. Apoptosis, a controlled and orderly programmed cell death regulated by genes, helps eliminate unnecessary or abnormal cells and maintain internal environmental stability. It also regulates various cell functions and contributes to the development of many diseases. In wound healing, programmed cell death is essential for removing inflammatory cells and forming scars. On the other hand, necroptosis, another form of programmed cell death, has not been thoroughly investigated regarding its role in wound healing. This review explores the changes and apoptosis of specific cell groups during wound healing after an injury and delves into the potential underlying mechanisms. Furthermore, it briefly discusses the possible mechanisms linking wound inflammation and fibrosis to apoptosis in wound healing. By understanding the relationship between apoptosis and wound healing and investigating the molecular mechanisms involved in apoptosis regulation, new strategies for the clinical treatment of wound healing may be discovered.
{"title":"Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention","authors":"Xingqian Wu, Rifang Gu, Ming Tang, Xingrui Mu, Wenjie He, Xuqiang Nie","doi":"10.1093/burnst/tkae061","DOIUrl":"https://doi.org/10.1093/burnst/tkae061","url":null,"abstract":"Wound healing is a complex and multistep biological process that involves the cooperation of various cell types. Programmed cell death, including apoptosis and necrotizing apoptosis, plays a crucial role in this process. Apoptosis, a controlled and orderly programmed cell death regulated by genes, helps eliminate unnecessary or abnormal cells and maintain internal environmental stability. It also regulates various cell functions and contributes to the development of many diseases. In wound healing, programmed cell death is essential for removing inflammatory cells and forming scars. On the other hand, necroptosis, another form of programmed cell death, has not been thoroughly investigated regarding its role in wound healing. This review explores the changes and apoptosis of specific cell groups during wound healing after an injury and delves into the potential underlying mechanisms. Furthermore, it briefly discusses the possible mechanisms linking wound inflammation and fibrosis to apoptosis in wound healing. By understanding the relationship between apoptosis and wound healing and investigating the molecular mechanisms involved in apoptosis regulation, new strategies for the clinical treatment of wound healing may be discovered.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"52 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143020359","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}
Haibin Zhao, Zhigang Zhang, Hongyu Liu, Mingxiu Ma, Peng Sun, Yang Zhao, Xun Liu
In this review, we examine the significance of multi-omics technologies in understanding the plethora of intricate processes that activate gastrointestinal (GI) injury repair. Multi-omics, which includes genomics, transcriptomics, proteomics, and metabolomics, allows intricate mapping of cellular responses and molecular pathways involved in GI repair. We highlight the potential of multi-omics to discover previously unknown therapeutic targets or elucidate the molecular basis of the pathogenesis of GI. Furthermore, we explore the possibilities of integrating omics data to improve prediction models, and summarize the state-of-the-art technological developments and persisting obstacles that hinder the translation of multi-omics into clinical practice. Finally, innovative multi-omics approaches that can improve patient outcomes and advance therapeutic strategies in GI medicine are discussed.
{"title":"Multi-omics perspective: mechanisms of gastrointestinal injury repair","authors":"Haibin Zhao, Zhigang Zhang, Hongyu Liu, Mingxiu Ma, Peng Sun, Yang Zhao, Xun Liu","doi":"10.1093/burnst/tkae057","DOIUrl":"https://doi.org/10.1093/burnst/tkae057","url":null,"abstract":"In this review, we examine the significance of multi-omics technologies in understanding the plethora of intricate processes that activate gastrointestinal (GI) injury repair. Multi-omics, which includes genomics, transcriptomics, proteomics, and metabolomics, allows intricate mapping of cellular responses and molecular pathways involved in GI repair. We highlight the potential of multi-omics to discover previously unknown therapeutic targets or elucidate the molecular basis of the pathogenesis of GI. Furthermore, we explore the possibilities of integrating omics data to improve prediction models, and summarize the state-of-the-art technological developments and persisting obstacles that hinder the translation of multi-omics into clinical practice. Finally, innovative multi-omics approaches that can improve patient outcomes and advance therapeutic strategies in GI medicine are discussed.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"105 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992160","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}
Background Skin innervation is very important for normal wound healing, and receptor activity-modifying protein 1 (RAMP1) has been reported to modulate calcitonin gene-related peptide (CGRP) receptor function and thus be a potential treatment target. This study aimed to elucidate the intricate regulatory effect of RAMP1 on skin fibroblast function, thereby addressing the existing knowledge gap in this area. Methods Immunohistochemical staining and immunofluorescence (IF) staining were used to measure the dynamic changes in the expression of RAMP1 and α-smooth muscle actin (α-SMA) in skin wound tissue in mice. Mouse skin fibroblasts (MSFs) stably transfected with Tet-on-Flag-RAMP1 overexpression (OE) and Tet-on-Flag control (Ctrl) lentiviruses were constructed for in vitro experiments. High mobility group AT-hook 1 (HMGA1) plasmids and α-SMA plasmids were used to overexpress HMGA1 and α-SMA, respectively. An α-SMA siRNA was used to silence α-SMA. Quantitative real-time polymerase chain reaction (qPCR), western blot and IF staining analyses were used to determine the mRNA and protein levels in the cells in different groups. A scratch wound healing assay was used to evaluate the cell migration ability of different groups. Cleavage under targets and release using nuclease (CUT & RUN) assays and dual-luciferase reporter assays were used to predict and verify the interaction between HMGA1 and the α-SMA promoter. Results RAMP1 and α-SMA protein expression levels in the dermis changed dynamically and were negatively correlated during dorsal skin wound healing in mice. RAMP1 OE in vitro inhibited the differentiation and promoted the migration of MSFs by decreasing α-SMA expression via the suppression of HMGA1, which was shown for the first time to bind to the α-SMA promoter and increase α-SMA transcription. RAMP1 OE also modulated extracellular matrix (ECM) synthesis and remodeling by promoting collagen III and MMP9 expression and decreasing collagen I, MMP2, and tissue inhibitor of metalloproteinases 1 expression. Conclusions Our findings suggest that RAMP1 OE decreases differentiation and promotes migration in MSFs by downregulating α-SMA expression via the suppression of HMGA1 and modulates ECM synthesis and remodeling, revealing a novel mechanism regulating α-SMA transcription, providing new insights into the RAMP1-mediated regulation of fibroblast function, and identifying effective nerve-related targets for skin wound repair.
{"title":"Receptor activity-modifying protein 1 regulates the differentiation of mouse skin fibroblasts by downregulating α-SMA expression via suppression of high mobility group AT-hook 1 to promote skin wound repair","authors":"Ru Song, Jiaxu Ma, Siyuan Yin, Zhenjie Wu, Chunyan Liu, Rui Sun, Guoqi Cao, Yongpan Lu, Jian Liu, Linqi Su, Yibing Wang","doi":"10.1093/burnst/tkae068","DOIUrl":"https://doi.org/10.1093/burnst/tkae068","url":null,"abstract":"Background Skin innervation is very important for normal wound healing, and receptor activity-modifying protein 1 (RAMP1) has been reported to modulate calcitonin gene-related peptide (CGRP) receptor function and thus be a potential treatment target. This study aimed to elucidate the intricate regulatory effect of RAMP1 on skin fibroblast function, thereby addressing the existing knowledge gap in this area. Methods Immunohistochemical staining and immunofluorescence (IF) staining were used to measure the dynamic changes in the expression of RAMP1 and α-smooth muscle actin (α-SMA) in skin wound tissue in mice. Mouse skin fibroblasts (MSFs) stably transfected with Tet-on-Flag-RAMP1 overexpression (OE) and Tet-on-Flag control (Ctrl) lentiviruses were constructed for in vitro experiments. High mobility group AT-hook 1 (HMGA1) plasmids and α-SMA plasmids were used to overexpress HMGA1 and α-SMA, respectively. An α-SMA siRNA was used to silence α-SMA. Quantitative real-time polymerase chain reaction (qPCR), western blot and IF staining analyses were used to determine the mRNA and protein levels in the cells in different groups. A scratch wound healing assay was used to evaluate the cell migration ability of different groups. Cleavage under targets and release using nuclease (CUT & RUN) assays and dual-luciferase reporter assays were used to predict and verify the interaction between HMGA1 and the α-SMA promoter. Results RAMP1 and α-SMA protein expression levels in the dermis changed dynamically and were negatively correlated during dorsal skin wound healing in mice. RAMP1 OE in vitro inhibited the differentiation and promoted the migration of MSFs by decreasing α-SMA expression via the suppression of HMGA1, which was shown for the first time to bind to the α-SMA promoter and increase α-SMA transcription. RAMP1 OE also modulated extracellular matrix (ECM) synthesis and remodeling by promoting collagen III and MMP9 expression and decreasing collagen I, MMP2, and tissue inhibitor of metalloproteinases 1 expression. Conclusions Our findings suggest that RAMP1 OE decreases differentiation and promotes migration in MSFs by downregulating α-SMA expression via the suppression of HMGA1 and modulates ECM synthesis and remodeling, revealing a novel mechanism regulating α-SMA transcription, providing new insights into the RAMP1-mediated regulation of fibroblast function, and identifying effective nerve-related targets for skin wound repair.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"137 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991904","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}
Diabetes mellitus is a group of chronic metabolic diseases worldwide seriously threatens human health and increases social and economic burden; underlying drivers of impaired healing include uncontrolled inflammation, repeated ischemia–reperfusion injury, and neuropathy alongside infection risks. Macrophages orchestrate standard repair, exhibit sustained classical pro-inflammatory activation in diabetes, disrupting growth factor secretion, angiogenesis, and matrix regulation. Hyperglycemia- mediated advanced glycation end products and reactive oxygen species heighten pattern recognition receptor stimulation, causing reduced alternative macrophage differentiation. Promising immunomodulation approaches redirecting their phenotypes to resolve inflammation and stimulate regeneration provides optimism. We discuss macrophage origination, polarization dynamics, diabetic wound phenotypic imbalance, and critical microenvironmental disruptions perpetuating pathological function. Elucidating specific regulatory nodes upholding their activation states will inform intelligent targeting opportunities. Overall, infiltrating macrophages constitute indispensable yet amenable diabetic wound healing coordinators.
{"title":"Masterful macrophages: understanding and targeting activation dysfunction in diabetic wounds","authors":"Linian Peng, Gaoxing Luo, Weifeng He, Guangping Liang","doi":"10.1093/burnst/tkaf003","DOIUrl":"https://doi.org/10.1093/burnst/tkaf003","url":null,"abstract":"Diabetes mellitus is a group of chronic metabolic diseases worldwide seriously threatens human health and increases social and economic burden; underlying drivers of impaired healing include uncontrolled inflammation, repeated ischemia–reperfusion injury, and neuropathy alongside infection risks. Macrophages orchestrate standard repair, exhibit sustained classical pro-inflammatory activation in diabetes, disrupting growth factor secretion, angiogenesis, and matrix regulation. Hyperglycemia- mediated advanced glycation end products and reactive oxygen species heighten pattern recognition receptor stimulation, causing reduced alternative macrophage differentiation. Promising immunomodulation approaches redirecting their phenotypes to resolve inflammation and stimulate regeneration provides optimism. We discuss macrophage origination, polarization dynamics, diabetic wound phenotypic imbalance, and critical microenvironmental disruptions perpetuating pathological function. Elucidating specific regulatory nodes upholding their activation states will inform intelligent targeting opportunities. Overall, infiltrating macrophages constitute indispensable yet amenable diabetic wound healing coordinators.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"11 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992575","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}
Zhuo Liu, Kang Wu, Hong Zeng, Wenxin Huang, Xuemeng Wang, Ying Qu, Chuntao Chen, Lei Zhang, Dongpin Sun, Sifeng Chen, Xiao Lin, Ning Sun, Lei Yang, Chen Xu
Background Magnesium ions play crucial roles in maintaining cellular functions. Research has shown that Mg2+ can promote angiogenesis, indicating its potential for treating cardiovascular ischemic diseases. However, conventional intravenous or oral administration of Mg2+ presents several challenges, including the risk of systemic side effects, diminished bioavailability, and a lack of targeted delivery mechanisms. In this study, we designed a Mg2+-releasing adhesive tissue patch (MgAP) that enables the dural release of Mg2+ ions. Methods A novel Mg2+-releasing adhesive patch (MgAP) was developed on the basis of ionic crosslinking. Fourier transform infrared spectroscopy confirmed the chemical structure, whereas rheological analysis demonstrated stable mechanical properties and adaptability to dynamic loads. Sustained Mg2+ release was quantified over 7 days by inductively coupled plasma–mass spectrometry. In a rat acute myocardial infarction model, we performed echocardiography and strain analysis to assess cardiac function and histological staining to evaluate adverse remodeling. We also verified the proangiogenic effect through in vitro tube formation and in vivo immunofluorescence assays. Furthermore, transcriptomics and Western blotting were performed to explore the underlying mechanism. Additional assessments were also carried out in a rat model of lower limb ischemia. Results Compared with intravenous administration of magnesium chloride, MgAP application effectively improved cardiac function and reduced adverse remodeling in the myocardial infarction rat model. The left ventricular ejection fraction increased by 20.3 ± 6.6%, and the cardiac radial strain improved by 27.4 ± 4.1%. The cardiac fibrosis area and cell apoptosis rate decreased by 10.9 ± 1.2% and 32.1 ± 5.5%, respectively. RNA sequencing analysis also highlighted the upregulation of genes related to cardiac electrophysiological properties, structural and functional intercellular connections, and revascularization. The increased gap junction protein expression and restored local blood supply could contribute to the cardiac repair process posttreatment. The proangiogenic effect of MgAP was also observed in the rat limb ischemia model. Conclusions The above results revealed the convincing vascular regeneration effect of an ion therapy-based hydrogel, which enabled the local delivery of Mg2+ to the targeted ischemic tissue, aiding in cardiac and lower limb repair. This study presents a novel strategy and highlights its potential for use across various ischemic conditions.
{"title":"A bioactive Hydrogel Patch Accelerates Revascularization in Ischemic Lesions for Tissue Repair","authors":"Zhuo Liu, Kang Wu, Hong Zeng, Wenxin Huang, Xuemeng Wang, Ying Qu, Chuntao Chen, Lei Zhang, Dongpin Sun, Sifeng Chen, Xiao Lin, Ning Sun, Lei Yang, Chen Xu","doi":"10.1093/burnst/tkaf005","DOIUrl":"https://doi.org/10.1093/burnst/tkaf005","url":null,"abstract":"Background Magnesium ions play crucial roles in maintaining cellular functions. Research has shown that Mg2+ can promote angiogenesis, indicating its potential for treating cardiovascular ischemic diseases. However, conventional intravenous or oral administration of Mg2+ presents several challenges, including the risk of systemic side effects, diminished bioavailability, and a lack of targeted delivery mechanisms. In this study, we designed a Mg2+-releasing adhesive tissue patch (MgAP) that enables the dural release of Mg2+ ions. Methods A novel Mg2+-releasing adhesive patch (MgAP) was developed on the basis of ionic crosslinking. Fourier transform infrared spectroscopy confirmed the chemical structure, whereas rheological analysis demonstrated stable mechanical properties and adaptability to dynamic loads. Sustained Mg2+ release was quantified over 7 days by inductively coupled plasma–mass spectrometry. In a rat acute myocardial infarction model, we performed echocardiography and strain analysis to assess cardiac function and histological staining to evaluate adverse remodeling. We also verified the proangiogenic effect through in vitro tube formation and in vivo immunofluorescence assays. Furthermore, transcriptomics and Western blotting were performed to explore the underlying mechanism. Additional assessments were also carried out in a rat model of lower limb ischemia. Results Compared with intravenous administration of magnesium chloride, MgAP application effectively improved cardiac function and reduced adverse remodeling in the myocardial infarction rat model. The left ventricular ejection fraction increased by 20.3 ± 6.6%, and the cardiac radial strain improved by 27.4 ± 4.1%. The cardiac fibrosis area and cell apoptosis rate decreased by 10.9 ± 1.2% and 32.1 ± 5.5%, respectively. RNA sequencing analysis also highlighted the upregulation of genes related to cardiac electrophysiological properties, structural and functional intercellular connections, and revascularization. The increased gap junction protein expression and restored local blood supply could contribute to the cardiac repair process posttreatment. The proangiogenic effect of MgAP was also observed in the rat limb ischemia model. Conclusions The above results revealed the convincing vascular regeneration effect of an ion therapy-based hydrogel, which enabled the local delivery of Mg2+ to the targeted ischemic tissue, aiding in cardiac and lower limb repair. This study presents a novel strategy and highlights its potential for use across various ischemic conditions.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"45 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991903","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}
Fanglin Shao, Zhipeng Wang, Luxia Ye, Ruicheng Wu, Jie Wang, Qing-Xin Yu, Dilinaer Wusiman, Zhouting Tuo, Koo Han Yoo, Ziyu Shu, Wuran Wei, Dengxiong Li, William C Cho, Zhihong Liu, Dechao Feng
The circadian clock is an internal timekeeper system that regulates biological processes through a central circadian clock and peripheral clocks controlling various genes. Basic helix–loop–helix ARNT-like 1 (BMAL1), also known as aryl hydrocarbon receptor nuclear translocator-like protein 1 (ARNTL1), is a key component of the circadian clock. The deletion of BMAL1 alone can abolish the circadian rhythms of the human body. BMAL1 plays a critical role in immune cell function. Dysregulation of BMAL1 is linked to immune-related diseases such as autoimmune diseases, infectious diseases, and cancer, and vice versa. This review highlights the significant role of BMAL1 in governing immune cells, including their development, differentiation, migration, homing, metabolism, and effector functions. This study also explores how dysregulation of BMAL1 can have far-reaching implications and potentially contribute to the onset of immune-related diseases such as autoimmune diseases, infectious diseases, cancer, sepsis, and trauma. Furthermore, this review discusses treatments for immune-related diseases that target BMAL1 disorders. Understanding the impact of BMAL1 on immune function can provide insights into the pathogenesis of immune-related diseases and help in the development of more effective treatment strategies. Targeting BMAL1 has been demonstrated to achieve good efficacy in immune-related diseases, indicating its promising potential as a targetable therapeutic target in these diseases.
{"title":"Basic helix–loop–helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases","authors":"Fanglin Shao, Zhipeng Wang, Luxia Ye, Ruicheng Wu, Jie Wang, Qing-Xin Yu, Dilinaer Wusiman, Zhouting Tuo, Koo Han Yoo, Ziyu Shu, Wuran Wei, Dengxiong Li, William C Cho, Zhihong Liu, Dechao Feng","doi":"10.1093/burnst/tkae075","DOIUrl":"https://doi.org/10.1093/burnst/tkae075","url":null,"abstract":"The circadian clock is an internal timekeeper system that regulates biological processes through a central circadian clock and peripheral clocks controlling various genes. Basic helix–loop–helix ARNT-like 1 (BMAL1), also known as aryl hydrocarbon receptor nuclear translocator-like protein 1 (ARNTL1), is a key component of the circadian clock. The deletion of BMAL1 alone can abolish the circadian rhythms of the human body. BMAL1 plays a critical role in immune cell function. Dysregulation of BMAL1 is linked to immune-related diseases such as autoimmune diseases, infectious diseases, and cancer, and vice versa. This review highlights the significant role of BMAL1 in governing immune cells, including their development, differentiation, migration, homing, metabolism, and effector functions. This study also explores how dysregulation of BMAL1 can have far-reaching implications and potentially contribute to the onset of immune-related diseases such as autoimmune diseases, infectious diseases, cancer, sepsis, and trauma. Furthermore, this review discusses treatments for immune-related diseases that target BMAL1 disorders. Understanding the impact of BMAL1 on immune function can provide insights into the pathogenesis of immune-related diseases and help in the development of more effective treatment strategies. Targeting BMAL1 has been demonstrated to achieve good efficacy in immune-related diseases, indicating its promising potential as a targetable therapeutic target in these diseases.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"49 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142988609","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}
Chronic leg wounds represent a major burden of disease worldwide, costing health care systems billions of dollars each year. Aside from the financial implications, they also impose a significant physical and psychosocial burden on the patient, their relatives and/or carers, and the community. Whilst measures such as maintenance of wound hygiene, debridement, dressings and compression are the current standard of care, complete healing is not always achievable and ulcer recurrence is common. Thus, there is still a gap to breach in terms of understanding the intricate pathophysiology of chronic wounds and the role this plays on treatment and management. Pseudomonas aeruginosa has been linked to poor wound healing, with the pathogen being frequently isolated from chronic leg ulcers. Characterized by its multi-drug resistance, targeting P. aeruginosa requires the development of novel therapeutic options. Thus, the aim of this literature review is to describe the pathophysiology of P. aeruginosa in chronic leg ulcers and discuss novel treatment strategies. Here, we describe the key molecular mechanisms driving the observed clinical effect of P. aeruginosa on wounds and discuss novel strategies of molecular targeting of this common bacteria, establishing new approaches that could benefit patients with chronic hard to heal wounds.
{"title":"Understanding the pathophysiology of Pseudomonas aeruginosa colonization as a guide for future treatment for chronic leg ulcers","authors":"Gabriela Gonzalez Matheus, Michelle N Chamoun, Kiarash Khosrotehrani, Yogeesan Sivakumaran, Timothy J Wells","doi":"10.1093/burnst/tkae083","DOIUrl":"https://doi.org/10.1093/burnst/tkae083","url":null,"abstract":"Chronic leg wounds represent a major burden of disease worldwide, costing health care systems billions of dollars each year. Aside from the financial implications, they also impose a significant physical and psychosocial burden on the patient, their relatives and/or carers, and the community. Whilst measures such as maintenance of wound hygiene, debridement, dressings and compression are the current standard of care, complete healing is not always achievable and ulcer recurrence is common. Thus, there is still a gap to breach in terms of understanding the intricate pathophysiology of chronic wounds and the role this plays on treatment and management. Pseudomonas aeruginosa has been linked to poor wound healing, with the pathogen being frequently isolated from chronic leg ulcers. Characterized by its multi-drug resistance, targeting P. aeruginosa requires the development of novel therapeutic options. Thus, the aim of this literature review is to describe the pathophysiology of P. aeruginosa in chronic leg ulcers and discuss novel treatment strategies. Here, we describe the key molecular mechanisms driving the observed clinical effect of P. aeruginosa on wounds and discuss novel strategies of molecular targeting of this common bacteria, establishing new approaches that could benefit patients with chronic hard to heal wounds.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"99 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142988610","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：