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The impact of burn injury on the central nervous system 烧伤对中枢神经系统的影响
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-02-02 DOI: 10.1093/burnst/tkad037
Amira Allahham, Grant Rowe, Andrew Stevenson, Mark W Fear, Ann-Maree Vallence, Fiona M Wood
Burn injuries can be devastating, with life-long impacts including an increased risk of hospitalization for a wide range of secondary morbidities. One area that remains not fully understood is the impact of burn trauma on the central nervous system (CNS). This review will outline the current findings on the physiological impact that burns have on the CNS and how this may contribute to the development of neural comorbidities including mental health conditions. This review highlights the damaging effects caused by burn injuries on the CNS, characterized by changes to metabolism, molecular damage to cells and their organelles, and disturbance to sensory, motor and cognitive functions in the CNS. This damage is likely initiated by the inflammatory response that accompanies burn injury, and it is often long-lasting. Treatments used to relieve the symptoms of damage to the CNS due to burn injury often target inflammatory pathways. However, there are non-invasive treatments for burn patients that target the functional and cognitive damage caused by the burn, including transcranial magnetic stimulation and virtual reality. Future research should focus on understanding the mechanisms that underpin the impact of a burn injury on the CNS, burn severity thresholds required to inflict damage to the CNS, and acute and long-term therapies to ameliorate deleterious CNS changes after a burn.
烧伤可能是毁灭性的,会造成终生影响,包括增加因各种继发性疾病住院的风险。烧伤创面对中枢神经系统(CNS)的影响是人们尚未完全了解的一个领域。本综述将概述目前关于烧伤对中枢神经系统生理影响的研究结果,以及这可能如何导致神经系统合并症(包括精神疾病)的发展。本综述强调了烧伤对中枢神经系统造成的破坏性影响,其特点是新陈代谢发生变化,细胞及其细胞器受到分子损伤,中枢神经系统的感觉、运动和认知功能受到干扰。这种损伤可能是由烧伤伴随的炎症反应引起的,而且往往持续时间较长。用于缓解烧伤导致的中枢神经系统损伤症状的治疗通常以炎症通路为目标。不过,也有针对烧伤造成的功能和认知损伤的非侵入性治疗方法,包括经颅磁刺激和虚拟现实。未来的研究应侧重于了解烧伤对中枢神经系统的影响机制、对中枢神经系统造成损害所需的烧伤严重程度阈值,以及改善烧伤后中枢神经系统有害变化的急性和长期疗法。
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引用次数: 0
Consensus on the treatment of second-degree burn wounds (2024 edition). 二度烧伤治疗共识(2024 年版)。
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-01-30 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkad061
Shizhao Ji, Shichu Xiao, Zhaofan Xia

Second-degree burns are the most common type of burn in clinical practice and hard to manage. Their treatment requires not only a consideration of the different outcomes that may arise from the dressing changes or surgical therapies themselves but also an evaluation of factors such as the burn site, patient age and burn area. Meanwhile, special attention should be given to the fact that there is no unified standard or specification for the diagnosis, classification, surgical procedure, and infection diagnosis and grading of second-degree burn wounds. This not only poses great challenges to the formulation of clinical treatment plans but also significantly affects the consistency of clinical studies. Moreover, currently, there are relatively few guidelines or expert consensus for the management of second-degree burn wounds, and no comprehensive and systematic guidelines or specifications for the treatment of second-degree burns have been formed. Therefore, we developed the Consensus on the Treatment of Second-Degree Burn Wounds (2024 edition), based on evidence-based medicine and expert opinion. This consensus provides specific recommendations on prehospital first aid, nonsurgical treatment, surgical treatment and infection treatment for second-degree burns. The current consensus generated a total of 58 recommendations, aiming to form a standardized clinical treatment plan.

二度烧伤是临床上最常见的烧伤类型,也是最难处理的烧伤。其治疗不仅需要考虑换药或手术疗法本身可能导致的不同结果,还需要对烧伤部位、患者年龄和烧伤面积等因素进行评估。同时,需要特别注意的是,目前对于二度烧伤创面的诊断、分类、手术方法、感染诊断和分级还没有统一的标准或规范。这不仅给临床治疗方案的制定带来了巨大挑战,也极大地影响了临床研究的一致性。此外,目前针对二度烧伤创面处理的指南或专家共识较少,尚未形成全面系统的二度烧伤治疗指南或规范。因此,我们在循证医学和专家意见的基础上,制定了《二度烧伤创面救治共识(2024 年版)》。该共识就二度烧伤的院前急救、非手术治疗、手术治疗和感染治疗提出了具体建议。本次共识共提出 58 项建议,旨在形成标准化的临床治疗方案。
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引用次数: 0
Broadening horizons: ferroptosis as a new target for traumatic brain injury 拓宽视野:作为脑外伤治疗新靶点的铁蛋白沉积症
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-01-21 DOI: 10.1093/burnst/tkad051
Ziqing Wei, Haihan Yu, Huijuan Zhao, Mingze Wei, Han Xing, Jinyan Pei, Yang Yang, Kaidi Ren
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, with ~50 million people experiencing TBI each year. Ferroptosis, a form of regulated cell death triggered by iron ion-catalyzed and reactive oxygen species-induced lipid peroxidation, has been identified as a potential contributor to traumatic central nervous system conditions, suggesting its involvement in the pathogenesis of TBI. Alterations in iron metabolism play a crucial role in secondary injury following TBI. This study aimed to explore the role of ferroptosis in TBI, focusing on iron metabolism disorders, lipid metabolism disorders and the regulatory axis of system Xc−/glutathione/glutathione peroxidase 4 in TBI. Additionally, we examined the involvement of ferroptosis in the chronic TBI stage. Based on these findings, we discuss potential therapeutic interventions targeting ferroptosis after TBI. In conclusion, this review provides novel insights into the pathology of TBI and proposes potential therapeutic targets.
创伤性脑损伤(TBI)是导致全球死亡和残疾的主要原因,每年约有 5000 万人受到创伤性脑损伤。铁变态反应是一种由铁离子催化和活性氧诱导的脂质过氧化反应引发的调节性细胞死亡,已被确认为创伤性中枢神经系统疾病的潜在诱因,这表明铁变态反应与创伤性脑损伤的发病机制有关。铁代谢的改变在创伤性脑损伤后的继发性损伤中起着至关重要的作用。本研究旨在探讨铁变态反应在创伤性脑损伤中的作用,重点是铁代谢紊乱、脂代谢紊乱和创伤性脑损伤中 Xc- 系统/谷胱甘肽/谷胱甘肽过氧化物酶 4 的调节轴。此外,我们还研究了慢性创伤性脑损伤阶段的铁变态反应。基于这些发现,我们讨论了针对创伤性脑损伤后铁蛋白沉积的潜在治疗干预措施。总之,本综述提供了对创伤性脑损伤病理的新见解,并提出了潜在的治疗目标。
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引用次数: 0
Exosomal miR-4645-5p from hypoxic bone marrow mesenchymal stem cells facilitates diabetic wound healing by restoring keratinocyte autophagy 缺氧骨髓间充质干细胞的外泌体 miR-4645-5p 通过恢复角质形成细胞的自噬作用促进糖尿病伤口愈合
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-01-19 DOI: 10.1093/burnst/tkad058
Yan Shi, Shang Wang, Dewu Liu, Zhengguang Wang, Yihan Zhu, Jun Li, Kui Xu, Furong Li, Huicai Wen, Ronghua Yang
Background Refractory diabetic wounds are a common occurrence in patients with diabetes and epidermis-specific macroautophagy/autophagy impairment has been implicated in their pathogenesis. Therefore, identifying and developing treatment strategies capable of normalizing epidermis-specific macroautophagy/autophagy could facilitate diabetic wound healing. The study aims to investigate the potential of bone marrow mesenchymal stem cell-derived exosomes (BMSC-exos) from hypoxic conditions as a treatment to normalize epidermis-specific autophagy for diabetic wound healing. Methods We compared the effects of bone marrow mesenchymal stem cell (BMSC)-sourced exosomes (BMSC-Exos) from hypoxic conditions to those of BMSC in normoxic conditions (noBMSC-Exos). Our studies involved morphometric assessment of the exosomes, identification of the microRNA (miRNA) responsible for the effects, evaluation of keratinocyte functions and examination of effects of the exosomes on several molecules involved in the autophagy pathway such as microtubule-associated protein 1 light chain 3 beta, beclin 1, sequestosome 1, autophagy-related 5 and autophagy-related 5. The experiments used human BMSCs from the American Type Culture Collection, an in vivo mouse model of diabetes (db/db) to assess wound healing, as well as the human keratinocyte HaCaT cell line. In the methodology, the authors utilized an array of approaches that included electron microscopy, small interfering RNA (siRNA) studies, RNA in situ hybridization, quantitative real-time reverse transcription PCR (qRT-PCR), the isolation, sequencing and differential expression of miRNAs, as well as the use of miR-4645-5p-specific knockdown with an inhibitor. Results Hypoxia affected the release of exosomes from hypoxic BMSCs (hy-BMSCs) and influenced the size and morphology of the exosomes. Moreover, hyBMSC-Exo treatment markedly improved keratinocyte function, including keratinocyte autophagy, proliferation and migration. miRNA microarray and bioinformatics analysis showed that the target genes of the differentially expressed miRNAs were mainly enriched in ‘autophagy’ and ‘process utilizing autophagic mechanism’ in the ‘biological process’ category and miR-4645-5p as a major contributor to the pro-autophagy effect of hyBMSC-Exos. Moreover, mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2) was identified as a potential target of exosomal miR-4645-5p; this was confirmed using a dual luciferase assay. Exosomal miR-4645-5p mediates the inactivation of the MAPKAPK2-induced AKT kinase group (comprising AKT1, AKT2, and AKT3), which in turn suppresses AKT-mTORC1 signaling, thereby facilitating miR-4645-5p-mediated autophagy. Conclusions Overall, the results of this study showed that hyBMSC-Exo-mediated transfer of miR-4645-5p inactivated MAPKAPK2-induced AKT-mTORC1 signaling in keratinocytes, which activated keratinocyte autophagy, proliferation and migration, resulting in diabetic wound healing in mice. C
背景难治性糖尿病伤口是糖尿病患者的常见病,表皮特异性大自噬/自噬功能障碍与伤口的发病机制有关。因此,确定和开发能够使表皮特异性大自噬/自噬正常化的治疗策略可促进糖尿病伤口愈合。本研究旨在探讨缺氧条件下骨髓间充质干细胞衍生的外泌体(BMSC-exos)作为一种治疗方法使表皮特异性自噬正常化以促进糖尿病伤口愈合的潜力。方法 我们比较了缺氧条件下骨髓间充质干细胞(BMSC)来源的外泌体(BMSC-Exos)与常氧条件下骨髓间充质干细胞来源的外泌体(noBMSC-Exos)的效果。我们的研究包括对外泌体进行形态学评估、鉴定产生影响的微RNA (miRNA)、评估角质形成细胞的功能以及检查外泌体对参与自噬途径的几种分子的影响,如微管相关蛋白1轻链3 beta、beclin 1、sequestosome 1、自噬相关5和自噬相关5。实验使用了来自美国类型培养物保藏中心的人类 BMSCs、用于评估伤口愈合的糖尿病(db/db)体内小鼠模型以及人类角质细胞 HaCaT 细胞系。在研究方法上,作者采用了一系列方法,包括电子显微镜、小干扰 RNA(siRNA)研究、RNA 原位杂交、定量实时逆转录 PCR(qRT-PCR)、miRNA 的分离、测序和差异表达,以及使用抑制剂敲除 miR-4645-5p。结果 缺氧影响缺氧 BMSCs(hy-BMSCs)外泌体的释放,并影响外泌体的大小和形态。miRNA 微阵列和生物信息学分析表明,差异表达 miRNA 的靶基因主要富集在 "生物过程 "类别中的 "自噬 "和 "利用自噬机制的过程",而 miR-4645-5p 是 hyBMSC-Exos 促进自噬作用的主要贡献者。此外,有丝分裂原活化蛋白激酶活化蛋白激酶2(MAPKAPK2)被确定为外泌体miR-4645-5p的潜在靶标;这一点已通过双荧光素酶测定法得到证实。外泌体 miR-4645-5p 可介导 MAPKAPK2 诱导的 AKT 激酶组(包括 AKT1、AKT2 和 AKT3)失活,进而抑制 AKT-mTORC1 信号传导,从而促进 miR-4645-5p 介导的自噬。结论 总的来说,这项研究的结果表明,hyBMSC-Exo 介导的 miR-4645-5p 转移使角质形成细胞中 MAPKAPK2 诱导的 AKT-mTORC1 信号失活,从而激活了角质形成细胞的自噬、增殖和迁移,导致小鼠糖尿病伤口愈合。总之,这些发现有助于开发治疗糖尿病伤口的新策略。
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引用次数: 0
Inhibition of phosphatidylinositol 3-kinase catalytic subunit alpha by miR-203a-3p reduces hypertrophic scar formation via phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway. 通过 miR-203a-3p 抑制磷脂酰肌醇 3- 激酶催化亚基α,可减少通过磷脂酰肌醇 3- 激酶/AKT/mTOR 信号通路形成的肥厚性瘢痕。
IF 6.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-01-02 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkad048
Shixin Zhao, Hengdeng Liu, Hanwen Wang, Xuefeng He, Jinming Tang, Shaohai Qi, Ronghua Yang, Julin Xie

Background: Hypertrophic scar (HS) is a common fibroproliferative skin disease that currently has no truly effective therapy. Given the importance of phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) in hypertrophic scar formation, the development of therapeutic strategies for endogenous inhibitors against PIK3CA is of great interest. Here, we explored the molecular mechanisms underlying the protective effects of miR-203a-3p (PIK3CA inhibitor) against excessive scar.

Methods: Bioinformatic analysis, immunohistochemistry, immunofluorescence, miRNA screening and fluorescence in situ hybridization assays were used to identify the possible pathways and target molecules mediating HS formation. A series of in vitro and in vivo experiments were used to clarify the role of PIK3CA and miR-203a-3p in HS. Mechanistically, transcriptomic sequencing, immunoblotting, dual-luciferase assay and rescue experiments were executed.

Results: Herein, we found that PIK3CA and the phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR pathway were upregulated in scar tissues and positively correlated with fibrosis. We then identified miR-203a-3p as the most suitable endogenous inhibitor of PIK3CA. miR-203a-3p suppressed the proliferation, migration, collagen synthesis and contractility as well as the transdifferentiation of fibroblasts into myofibroblasts in vitro, and improved the morphology and histology of scars in vivo. Mechanistically, miR-203a-3p attenuated fibrosis by inactivating the PI3K/AKT/mTOR pathway by directly targeting PIK3CA.

Conclusions: PIK3CA and the PI3K/AKT/mTOR pathway are actively involved in scar fibrosis and miR-203a-3p might serve as a potential strategy for hypertrophic scar therapy through targeting PIK3CA and inactivating the PI3K/AKT/mTOR pathway.

背景:肥厚性疤痕(HS)是一种常见的纤维增生性皮肤病,目前尚无真正有效的治疗方法。鉴于磷脂酰肌醇 3- 激酶催化亚基α(PIK3CA)在肥厚性瘢痕形成中的重要性,开发针对 PIK3CA 的内源性抑制剂的治疗策略备受关注。在此,我们探讨了 miR-203a-3p(PIK3CA 抑制剂)对过度瘢痕具有保护作用的分子机制:方法:采用生物信息学分析、免疫组织化学、免疫荧光、miRNA 筛选和荧光原位杂交等方法来确定介导 HS 形成的可能途径和靶分子。一系列体外和体内实验明确了PIK3CA和miR-203a-3p在HS中的作用。从机理上讲,我们进行了转录组测序、免疫印迹、双荧光素酶检测和拯救实验:结果:我们发现 PIK3CA 和磷脂酰肌醇 3- 激酶(PI3K)/AKT/mTOR 通路在瘢痕组织中上调,并与纤维化呈正相关。miR-203a-3p 在体外抑制了成纤维细胞的增殖、迁移、胶原合成和收缩性,以及成纤维细胞向肌成纤维细胞的转分化,在体内改善了疤痕的形态和组织学。从机理上讲,miR-203a-3p通过直接靶向PIK3CA,使PI3K/AKT/mTOR通路失活,从而减轻了纤维化:结论:PIK3CA和PI3K/AKT/mTOR通路积极参与疤痕纤维化,miR-203a-3p通过靶向PIK3CA和使PI3K/AKT/mTOR通路失活,可能成为增生性疤痕治疗的潜在策略。
{"title":"Inhibition of phosphatidylinositol 3-kinase catalytic subunit alpha by miR-203a-3p reduces hypertrophic scar formation via phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway.","authors":"Shixin Zhao, Hengdeng Liu, Hanwen Wang, Xuefeng He, Jinming Tang, Shaohai Qi, Ronghua Yang, Julin Xie","doi":"10.1093/burnst/tkad048","DOIUrl":"10.1093/burnst/tkad048","url":null,"abstract":"<p><strong>Background: </strong>Hypertrophic scar (HS) is a common fibroproliferative skin disease that currently has no truly effective therapy. Given the importance of phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) in hypertrophic scar formation, the development of therapeutic strategies for endogenous inhibitors against PIK3CA is of great interest. Here, we explored the molecular mechanisms underlying the protective effects of miR-203a-3p (PIK3CA inhibitor) against excessive scar.</p><p><strong>Methods: </strong>Bioinformatic analysis, immunohistochemistry, immunofluorescence, miRNA screening and fluorescence <i>in situ</i> hybridization assays were used to identify the possible pathways and target molecules mediating HS formation. A series of <i>in vitro</i> and <i>in vivo</i> experiments were used to clarify the role of PIK3CA and miR-203a-3p in HS. Mechanistically, transcriptomic sequencing, immunoblotting, dual-luciferase assay and rescue experiments were executed.</p><p><strong>Results: </strong>Herein, we found that PIK3CA and the phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR pathway were upregulated in scar tissues and positively correlated with fibrosis. We then identified miR-203a-3p as the most suitable endogenous inhibitor of PIK3CA. miR-203a-3p suppressed the proliferation, migration, collagen synthesis and contractility as well as the transdifferentiation of fibroblasts into myofibroblasts <i>in vitro</i>, and improved the morphology and histology of scars <i>in vivo</i>. Mechanistically, miR-203a-3p attenuated fibrosis by inactivating the PI3K/AKT/mTOR pathway by directly targeting PIK3CA.</p><p><strong>Conclusions: </strong>PIK3CA and the PI3K/AKT/mTOR pathway are actively involved in scar fibrosis and miR-203a-3p might serve as a potential strategy for hypertrophic scar therapy through targeting PIK3CA and inactivating the PI3K/AKT/mTOR pathway.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkad048"},"PeriodicalIF":6.3,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139097378","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}
引用次数: 0
Metabolic reprogramming in skin wound healing. 皮肤伤口愈合过程中的代谢重编程。
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-01-02 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkad047
Zitong Wang, Feng Zhao, Chengcheng Xu, Qiqi Zhang, Haiyue Ren, Xing Huang, Cai He, Jiajie Ma, Zhe Wang

Metabolic reprogramming refers to the ability of a cell to alter its metabolism in response to different stimuli and forms of pressure. It helps cells resist external stress and provides them with new functions. Skin wound healing involves the metabolic reprogramming of nutrients, such as glucose, lipids, and amino acids, which play vital roles in the proliferation, differentiation, and migration of multiple cell types. During the glucose metabolic process in wounds, glucose transporters and key enzymes cause elevated metabolite levels. Glucose-mediated oxidative stress drives the proinflammatory response and promotes wound healing. Reprogramming lipid metabolism increases the number of fibroblasts and decreases the number of macrophages. It enhances local neovascularization and improves fibrin stability to promote extracellular matrix remodelling, accelerates wound healing, and reduces scar formation. Reprogramming amino acid metabolism affects wound re-epithelialization, collagen deposition, and angiogenesis. However, comprehensive reviews on the role of metabolic reprogramming in skin wound healing are lacking. Therefore, we have systematically reviewed the metabolic reprogramming of glucose, lipids, and amino acids during skin wound healing. Notably, we identified their targets with potential therapeutic value and elucidated their mechanisms of action.

代谢重编程是指细胞在不同刺激和压力下改变其新陈代谢的能力。它有助于细胞抵御外部压力,并为细胞提供新的功能。皮肤伤口愈合涉及葡萄糖、脂类和氨基酸等营养物质的新陈代谢重编程,这些营养物质在多种类型细胞的增殖、分化和迁移过程中发挥着重要作用。在伤口的葡萄糖代谢过程中,葡萄糖转运体和关键酶会导致代谢物水平升高。葡萄糖介导的氧化应激会推动促炎反应,促进伤口愈合。重新规划脂质代谢可增加成纤维细胞的数量,减少巨噬细胞的数量。它能增强局部新生血管,提高纤维蛋白的稳定性,从而促进细胞外基质重塑,加快伤口愈合,减少疤痕形成。重新规划氨基酸代谢会影响伤口的再上皮化、胶原沉积和血管生成。然而,目前还缺乏有关代谢重编程在皮肤伤口愈合中作用的全面综述。因此,我们系统回顾了皮肤伤口愈合过程中葡萄糖、脂类和氨基酸的代谢重编程。值得注意的是,我们确定了它们具有潜在治疗价值的靶点,并阐明了它们的作用机制。
{"title":"Metabolic reprogramming in skin wound healing.","authors":"Zitong Wang, Feng Zhao, Chengcheng Xu, Qiqi Zhang, Haiyue Ren, Xing Huang, Cai He, Jiajie Ma, Zhe Wang","doi":"10.1093/burnst/tkad047","DOIUrl":"10.1093/burnst/tkad047","url":null,"abstract":"<p><p>Metabolic reprogramming refers to the ability of a cell to alter its metabolism in response to different stimuli and forms of pressure. It helps cells resist external stress and provides them with new functions. Skin wound healing involves the metabolic reprogramming of nutrients, such as glucose, lipids, and amino acids, which play vital roles in the proliferation, differentiation, and migration of multiple cell types. During the glucose metabolic process in wounds, glucose transporters and key enzymes cause elevated metabolite levels. Glucose-mediated oxidative stress drives the proinflammatory response and promotes wound healing. Reprogramming lipid metabolism increases the number of fibroblasts and decreases the number of macrophages. It enhances local neovascularization and improves fibrin stability to promote extracellular matrix remodelling, accelerates wound healing, and reduces scar formation. Reprogramming amino acid metabolism affects wound re-epithelialization, collagen deposition, and angiogenesis. However, comprehensive reviews on the role of metabolic reprogramming in skin wound healing are lacking. Therefore, we have systematically reviewed the metabolic reprogramming of glucose, lipids, and amino acids during skin wound healing. Notably, we identified their targets with potential therapeutic value and elucidated their mechanisms of action.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkad047"},"PeriodicalIF":5.3,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139097379","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}
引用次数: 0
S-Nitrosylation-mediated coupling of DJ-1 with PTEN induces PI3K/AKT/mTOR pathway-dependent keloid formation S-亚硝基化介导的DJ-1与PTEN偶联诱导PI3K/AKT/mTOR通路依赖性瘢痕疙瘩的形成
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2023-12-19 DOI: 10.1093/burnst/tkad024
Dongming Lv, Zhongye Xu, Pu Cheng, Zhicheng Hu, Yunxian Dong, Yanchao Rong, Hailin Xu, Zhiyong Wang, Xiaoling Cao, Wuguo Deng, Bing Tang
Background Keloids are aberrant dermal wound healing characterized by invasive growth, extracellular matrix deposition, cytokine overexpression and easy recurrence. Many factors have been implicated as pathological causes of keloids, particularly hyperactive inflammation, tension alignment and genetic predisposition. S-Nitrosylation (SNO), a unique form of protein modification, is associated with the local inflammatory response but its function in excessive fibrosis and keloid formation remains unknown. We aimed to discover the association between protein SNO and keloid formation. Methods Normal and keloid fibroblasts were isolated from collected normal skin and keloid tissues. The obtained fibroblasts were cultured in DMEM supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. The effects of DJ-1 on cell proliferation, apoptosis, migration and invasion, and on the expression of proteins were assayed. TurboID-based proximity labelling and liquid chromatography-mass spectrometry were conducted to explore the potential targets of DJ-1. Biotin-switch assays and transnitrosylation reactions were used to detect protein SNO. Quantitative data were compared by two-tailed Student’s t test. Results We found that DJ-1 served as an essential positive modulator to facilitate keloid cell proliferation, migration and invasion. A higher S-nitrosylated DJ-1 (SNO-DJ-1) level was observed in keloids, and the effect of DJ-1 on keloids was dependent on SNO of the Cys106 residue of the DJ-1 protein. SNO-DJ-1 was found to increase the level of phosphatase and tensin homolog (PTEN) S-nitrosylated at its Cys136 residue via transnitrosylation in keloids, thus diminishing the phosphatase activity of PTEN and activating the PI3K/AKT/mTOR pathway. Furthermore, Cys106-mutant DJ-1 is refractory to SNO and abrogates DJ-1-PTEN coupling and the SNO of the PTEN protein, thus repressing the PI3K/AKT/mTOR pathway and alleviating keloid formation. Importantly, the biological effect of DJ-1 in keloids is dependent on the SNO-DJ-1/SNO-PTEN/PI3K/AKT/mTOR axis. Conclusions For the first time, this study demonstrated the effect of transnitrosylation from DJ-1 to PTEN on promoting keloid formation via the PI3K/AKT/mTOR signaling pathway, suggesting that SNO of DJ-1 may be a novel therapeutic target for keloid treatment.
背景瘢痕疙瘩是一种异常的真皮伤口愈合,其特点是侵入性生长、细胞外基质沉积、细胞因子过度表达和容易复发。许多因素被认为是瘢痕疙瘩的病理原因,尤其是过度活跃的炎症、张力排列和遗传易感性。S-亚硝基化(SNO)是蛋白质修饰的一种独特形式,与局部炎症反应有关,但其在过度纤维化和瘢痕疙瘩形成中的功能仍不清楚。我们旨在发现蛋白质 SNO 与瘢痕疙瘩形成之间的关联。方法 从采集的正常皮肤和瘢痕疙瘩组织中分离出正常和瘢痕疙瘩成纤维细胞。获得的成纤维细胞在添加了 10%胎牛血清和 1% 青霉素/链霉素的 DMEM 中培养。检测了 DJ-1 对细胞增殖、凋亡、迁移和侵袭以及蛋白质表达的影响。通过基于 TurboID 的接近标记和液相色谱-质谱联用技术来探索 DJ-1 的潜在靶标。生物素开关测定和反硝化反应用于检测蛋白质 SNO。定量数据通过双尾学生 t 检验进行比较。结果 我们发现,DJ-1 是促进瘢痕疙瘩细胞增殖、迁移和侵袭的重要正调控因子。在瘢痕疙瘩中观察到较高的S-亚硝基化DJ-1(SNO-DJ-1)水平,DJ-1对瘢痕疙瘩的作用依赖于DJ-1蛋白Cys106残基的SNO。研究发现,在瘢痕疙瘩中,SNO-DJ-1可通过反硝基化作用增加磷酸酶和天丝蛋白同源物(PTEN)在其Cys136残基上的S-亚硝基化水平,从而降低PTEN的磷酸酶活性并激活PI3K/AKT/mTOR通路。此外,Cys106突变的DJ-1对SNO具有耐受性,并能减弱DJ-1-PTEN耦合和PTEN蛋白的SNO,从而抑制PI3K/AKT/mTOR通路并缓解瘢痕疙瘩的形成。重要的是,DJ-1在瘢痕疙瘩中的生物效应依赖于SNO-DJ-1/SNO-PTEN/PI3K/AKT/mTOR轴。结论 本研究首次证明了 DJ-1 至 PTEN 的反硝基化作用通过 PI3K/AKT/mTOR 信号通路促进瘢痕疙瘩的形成,这表明 DJ-1 的 SNO 可能是治疗瘢痕疙瘩的新型治疗靶点。
{"title":"S-Nitrosylation-mediated coupling of DJ-1 with PTEN induces PI3K/AKT/mTOR pathway-dependent keloid formation","authors":"Dongming Lv, Zhongye Xu, Pu Cheng, Zhicheng Hu, Yunxian Dong, Yanchao Rong, Hailin Xu, Zhiyong Wang, Xiaoling Cao, Wuguo Deng, Bing Tang","doi":"10.1093/burnst/tkad024","DOIUrl":"https://doi.org/10.1093/burnst/tkad024","url":null,"abstract":"Background Keloids are aberrant dermal wound healing characterized by invasive growth, extracellular matrix deposition, cytokine overexpression and easy recurrence. Many factors have been implicated as pathological causes of keloids, particularly hyperactive inflammation, tension alignment and genetic predisposition. S-Nitrosylation (SNO), a unique form of protein modification, is associated with the local inflammatory response but its function in excessive fibrosis and keloid formation remains unknown. We aimed to discover the association between protein SNO and keloid formation. Methods Normal and keloid fibroblasts were isolated from collected normal skin and keloid tissues. The obtained fibroblasts were cultured in DMEM supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. The effects of DJ-1 on cell proliferation, apoptosis, migration and invasion, and on the expression of proteins were assayed. TurboID-based proximity labelling and liquid chromatography-mass spectrometry were conducted to explore the potential targets of DJ-1. Biotin-switch assays and transnitrosylation reactions were used to detect protein SNO. Quantitative data were compared by two-tailed Student’s t test. Results We found that DJ-1 served as an essential positive modulator to facilitate keloid cell proliferation, migration and invasion. A higher S-nitrosylated DJ-1 (SNO-DJ-1) level was observed in keloids, and the effect of DJ-1 on keloids was dependent on SNO of the Cys106 residue of the DJ-1 protein. SNO-DJ-1 was found to increase the level of phosphatase and tensin homolog (PTEN) S-nitrosylated at its Cys136 residue via transnitrosylation in keloids, thus diminishing the phosphatase activity of PTEN and activating the PI3K/AKT/mTOR pathway. Furthermore, Cys106-mutant DJ-1 is refractory to SNO and abrogates DJ-1-PTEN coupling and the SNO of the PTEN protein, thus repressing the PI3K/AKT/mTOR pathway and alleviating keloid formation. Importantly, the biological effect of DJ-1 in keloids is dependent on the SNO-DJ-1/SNO-PTEN/PI3K/AKT/mTOR axis. Conclusions For the first time, this study demonstrated the effect of transnitrosylation from DJ-1 to PTEN on promoting keloid formation via the PI3K/AKT/mTOR signaling pathway, suggesting that SNO of DJ-1 may be a novel therapeutic target for keloid treatment.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138770779","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}
引用次数: 0
The impact of gut microbiota changes on the intestinal mucus barrier in burned mice: a study using 16S rRNA and metagenomic sequencing. 肠道微生物群变化对烧伤小鼠肠道粘液屏障的影响:一项使用 16S rRNA 和元基因组测序的研究。
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2023-12-19 eCollection Date: 2023-01-01 DOI: 10.1093/burnst/tkad056
Xule Zha, Sen Su, Dan Wu, Panyang Zhang, Yan Wei, Shijun Fan, Qianying Huang, Xi Peng

Background: The gut microbiota is a complex ecosystem that plays a critical role in human health and disease. However, the relationship between gut microbiota and intestinal damage caused by burns is not well understood. The intestinal mucus layer is crucial for maintaining intestinal homeostasis and providing a physiological barrier against bacterial invasion. This study aims to investigate the impact of gut microbiota on the synthesis and degradation of intestinal mucus after burns and explore potential therapeutic targets for burn injury.

Methods: A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice. Subsequently, 16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn. Based on this, metagenomic sequencing was conducted on samples collected at days 1, 5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.

Results: Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice. Moreover, the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury, but gradually recovered to normal as the disease progressed. Specifically, there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns, but the abundance returned to normal on day 5. Conversely, the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction. Further analysis revealed that after a burn injury, bacteria capable of degrading mucus may utilize glycoside hydrolases, flagella and internalins to break down the mucus layer, while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.

Conclusions: Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota. Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases, flagella, internalins, etc. Probiotics may provide short-chain fatty acids (particularly butyrate) as an energy source for stressed intestinal epithelial cells, promote mucin synthesis and accelerate repair of mucus layer.

背景:肠道微生物群是一个复杂的生态系统,在人类健康和疾病中发挥着至关重要的作用。然而,人们对肠道微生物群与烧伤造成的肠道损伤之间的关系还不甚了解。肠道粘液层对维持肠道平衡和提供防止细菌入侵的生理屏障至关重要。本研究旨在探讨肠道微生物群对烧伤后肠粘液合成和降解的影响,并探索烧伤的潜在治疗靶点:方法:采用改良的组织病理学分级系统研究烧伤对小鼠结肠组织和肠粘液屏障的影响。随后,采用 16S 核糖体 RNA 测序分析烧伤后第 1-10 天肠道微生物群的变化。在此基础上,对第 1、5 和 10 天采集的样本进行了元基因组测序,以研究粘液相关微生物群的变化并探索潜在的内在机制:结果:我们的研究结果表明,小鼠烧伤后第 3 天,粘液屏障遭到破坏,细菌发生迁移。此外,小鼠的肠道微生物群在烧伤后第 1 到 3 天受到严重破坏,但随着病情的发展逐渐恢复正常。具体来说,烧伤后第 1 天,与粘蛋白降解相关的共生菌和致病菌的数量明显增加,但第 5 天又恢复正常。相反,与粘蛋白合成相关的益生菌的数量却发生了相反的变化。进一步分析表明,烧伤后,能够降解粘液的细菌可能会利用糖苷水解酶、鞭毛和内毒素来分解粘液层,而合成粘液的细菌可能会通过促进短链脂肪酸的产生来帮助恢复粘液层:结论:烧伤导致结肠粘液屏障破坏和肠道微生物群失调。一些共生菌和致病菌可能通过糖苷水解酶、鞭毛、内蛋白等参与粘蛋白降解。益生菌可提供短链脂肪酸(尤其是丁酸盐),作为受压肠道上皮细胞的能量来源,促进粘蛋白的合成,加快粘液层的修复。
{"title":"The impact of gut microbiota changes on the intestinal mucus barrier in burned mice: a study using 16S rRNA and metagenomic sequencing.","authors":"Xule Zha, Sen Su, Dan Wu, Panyang Zhang, Yan Wei, Shijun Fan, Qianying Huang, Xi Peng","doi":"10.1093/burnst/tkad056","DOIUrl":"10.1093/burnst/tkad056","url":null,"abstract":"<p><strong>Background: </strong>The gut microbiota is a complex ecosystem that plays a critical role in human health and disease. However, the relationship between gut microbiota and intestinal damage caused by burns is not well understood. The intestinal mucus layer is crucial for maintaining intestinal homeostasis and providing a physiological barrier against bacterial invasion. This study aims to investigate the impact of gut microbiota on the synthesis and degradation of intestinal mucus after burns and explore potential therapeutic targets for burn injury.</p><p><strong>Methods: </strong>A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice. Subsequently, 16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn. Based on this, metagenomic sequencing was conducted on samples collected at days 1, 5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.</p><p><strong>Results: </strong>Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice. Moreover, the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury, but gradually recovered to normal as the disease progressed. Specifically, there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns, but the abundance returned to normal on day 5. Conversely, the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction. Further analysis revealed that after a burn injury, bacteria capable of degrading mucus may utilize glycoside hydrolases, flagella and internalins to break down the mucus layer, while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.</p><p><strong>Conclusions: </strong>Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota. Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases, flagella, internalins, etc. Probiotics may provide short-chain fatty acids (particularly butyrate) as an energy source for stressed intestinal epithelial cells, promote mucin synthesis and accelerate repair of mucus layer.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"11 ","pages":"tkad056"},"PeriodicalIF":5.3,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10734567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138828325","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}
引用次数: 0
The clinical differentiation of blood culture-positive and -negative sepsis in burn patients: a retrospective cohort study 烧伤患者血培养阳性和阴性败血症的临床鉴别:一项回顾性队列研究
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2023-12-19 DOI: 10.1093/burnst/tkad031
Jaechul Yoon, Dohern Kym, Jun Hur, Jongsoo Park, Myongjin Kim, Yong Suk Cho, Wook Chun, Dogeon Yoon
Background Sepsis is a potentially life-threatening condition that occurs when the body’s response to infection leads to widespread inflammation and tissue damage. Negative cultures can make it difficult for clinicians to make a diagnosis and may raise questions about the validity of the definition of sepsis. In addition, the clinical distinctions between burn patients with blood culture-positive and -negative sepsis are also poorly understood. Therefore, this study aimed to examine the clinical differences between blood culture-positive and -negative sepsis in burn patients in order to improve the understanding of the pathophysiology and epidemiology of sepsis in this population. Methods This study had a retrospective design, and the participants were adults aged ≥18 years. Patients diagnosed with sepsis were divided into two groups based on their blood culture results within 1 week of sepsis diagnosis. Results We enrolled 1643 patients admitted to our institution’s burn intensive care unit between January 2010 and December 2021. pH, platelet count, bicarbonate and haematocrit were significant in both the positive and negative groups. However, lymphocyte, red cell distribution width and blood urea nitrogen were significant only in the positive group, whereas lactate dehydrogenase was significant only in the negative group. Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumonia are common gram-negative bacterial species, and Staphylococcus aureus and Staphylococcus epidermidis are common gram-positive bacterial species seen in burn patients with positive blood cultures. Carbapenem resistance was found to be associated with an unfavourable prognosis in gram-negative bacteria, with the exception of P. aeruginosa. Conclusions pH, platelet count, bicarbonate and haematocrit were routine biomarkers that demonstrated statistical significance in both groups. Lactate dehydrogenase was significant in the blood-negative group, while red cell distribution width, blood urea nitrogen and lymphocyte count were significant in the positive group. Furthermore, the most common causes of sepsis are gram-negative bacteria, including A. baumannii, K. pneumoniae and P. aeruginosa. Additionally, resistance to carbapenems is associated with unfavourable outcomes.
背景败血症是一种可能危及生命的疾病,当机体对感染的反应导致广泛的炎症和组织损伤时就会发生败血症。培养阴性会使临床医生难以做出诊断,并可能对败血症定义的有效性产生疑问。此外,人们对烧伤患者血培养阳性和阴性败血症之间的临床区别也知之甚少。因此,本研究旨在探讨烧伤患者血培养阳性和阴性败血症之间的临床差异,以加深对该人群败血症病理生理学和流行病学的了解。方法 本研究采用回顾性设计,参与者为年龄≥18 岁的成年人。根据败血症确诊后 1 周内的血液培养结果,将确诊为败血症的患者分为两组。pH 值、血小板计数、碳酸氢盐和血细胞比容在阳性组和阴性组均有显著性差异。然而,只有阳性组的淋巴细胞、红细胞分布宽度和血尿素氮有显著性差异,而只有阴性组的乳酸脱氢酶有显著性差异。鲍曼不动杆菌、铜绿假单胞菌和肺炎克雷伯菌是常见的革兰氏阴性菌种,金黄色葡萄球菌和表皮葡萄球菌是烧伤患者血液培养阳性中常见的革兰氏阳性菌种。除铜绿假单胞菌外,碳青霉烯耐药性与革兰氏阴性菌的不良预后有关。结论 pH 值、血小板计数、碳酸氢盐和血细胞比容是常规生物标志物,在两组中均有统计学意义。乳酸脱氢酶在血阴性组有显著意义,而红细胞分布宽度、血尿素氮和淋巴细胞计数在血阳性组有显著意义。此外,败血症最常见的病因是革兰氏阴性菌,包括鲍曼不动杆菌、肺炎双球菌和铜绿假单胞菌。此外,对碳青霉烯类抗生素的耐药性与不利的预后有关。
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引用次数: 0
Plasma lipidomics reveal systemic changes persistent throughout early life following a childhood burn injury 血浆脂质组学揭示了儿童烧伤后整个生命早期持续存在的系统性变化
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2023-12-07 DOI: 10.1093/burnst/tkad044
Eva Kierath, Monique Ryan, Elaine Holmes, Jeremy K Nicholson, Mark W Fear, Fiona M Wood, Luke Whiley, Nicola Gray
Background Non-severe paediatric burns can result in poor long-term health outcomes. This occurs even in cases with good acute burn-related outcomes, including minimal scarring. The mechanisms that underpin the transition from non-severe burn to sustained negative long-term health impacts are currently unknown. However, sustained metabolic and immune changes have been observed in paediatric burn studies, suggesting these changes may be important. The plasma lipidome consists of a rich pool of bioactive metabolites that play critical roles in systemic processes including molecular signalling and inflammation. We hypothesised that changes in the plasma lipidome may reflect underlying changes in health status and be linked to long-term health after burn trauma. Methods This study analysed the lipidome in children who had previously experienced a non-severe burn, compared to non-injured controls. Thirty-three participants were recruited between the ages of 5 and 8 years who had experienced a non-severe burn between the ages of 1 and 3 years. Plasma samples were also collected from a non-injured, healthy, age and gender matched control group (n = 21). Plasma lipids were measured using reversed-phase liquid chromatographymass spectrometery (LC-MS). Results In total 838 reproducible lipid species from 19 sub-classes passed quality control procedures and progressed to statistical analysis. Analysis of individual lipid metabolites showed significantly higher concentrations of lysophosphatidylethanolamines and phosphatidylethanolamines, and significantly lower concentrations in myristic, palmitic and palmitoleic acids in the plasma of those who had experienced burn injury compared to controls. Conclusion Long-term changes in the lipid profile may give insight into the mechanisms underlying poor long-term health subsequent to non-severe burn injury. Further work to investigate the relationship between long-term pathology and lipidomic changes may lead to a better understanding of the causes of secondary morbidity post-burn and to clinical intervention to reduce the long-term health burden of burn trauma.
背景非重度小儿烧伤可能导致不良的长期健康后果。即使在急性烧伤相关结果良好(包括瘢痕最小)的病例中也会出现这种情况。目前尚不清楚从非严重烧伤转变为持续的长期负面健康影响的机制。不过,在儿科烧伤研究中观察到了持续的新陈代谢和免疫变化,这表明这些变化可能很重要。血浆脂质体由丰富的生物活性代谢物组成,在包括分子信号传导和炎症在内的全身过程中发挥着关键作用。我们假设血浆脂质体的变化可能反映了健康状况的潜在变化,并与烧伤后的长期健康状况有关。方法 本研究分析了曾经历过非严重烧伤的儿童与未受伤的对照组儿童的血脂组。研究人员招募了 33 名年龄在 5 到 8 岁之间、在 1 到 3 岁之间经历过非严重烧伤的儿童。此外,还从未受损伤、健康、年龄和性别匹配的对照组(21 人)中采集了血浆样本。血浆脂质采用反相液相色谱-质谱法(LC-MS)进行测量。结果 共有 19 个亚类的 838 种可重复脂质通过了质量控制程序并进入统计分析。对单个脂质代谢物的分析表明,与对照组相比,烧伤患者血浆中溶血磷脂酰乙醇胺和磷脂酰乙醇胺的浓度明显较高,肉豆蔻酸、棕榈酸和棕榈油酸的浓度明显较低。结论 脂质谱的长期变化可能有助于了解非严重烧伤后长期健康状况不佳的机制。进一步研究长期病理变化与脂质组变化之间的关系,可能有助于更好地了解烧伤后继发性发病的原因,并有助于采取临床干预措施,减轻烧伤创伤对健康造成的长期负担。
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Burns & Trauma
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