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Activating autophagy promotes skin regeneration induced by mechanical stretch during tissue expansion. 在组织扩张过程中,激活自噬可促进机械拉伸诱导的皮肤再生。
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2024-02-07 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkad057
Jing Du, Wei Liu, Yajuan Song, Yu Zhang, Chen Dong, Shaoheng Xiong, Zhaosong Huang, Tong Wang, Jianke Ding, Qiang He, Zhou Yu, Xianjie Ma

Background: Tissue expansion, a technique in which skin regeneration is induced by mechanical stretch stimuli, is commonly used for tissue repair and reconstruction. In this study, we aimed to monitor the autophagy levels of expanded skin after the application of expansion stimuli and explore the effect of autophagy modulation on skin regeneration.

Methods: A rat scalp expansion model was established to provide a stable expanded skin response to mechanical stretch. Autophagy levels at different time points (6, 12, 24, 48 and 72 h after the last expansion) were detected via western blotting. The effect of autophagy regulation on skin regeneration during tissue expansion was evaluated via skin expansion efficiency assessment, western blotting, immunofluorescence staining, TUNEL staining and laser Doppler blood flow imaging.

Results: The autophagic flux reached its highest level 48 h after tissue expansion. Activating autophagy by rapamycin increased the area of expanded skin as well as the thicknesses of epidermis and dermis. Furthermore, activating autophagy accelerated skin regeneration during tissue expansion by enhancing the proliferation of cells and the number of epidermal basal and hair follicle stem cells, reducing apoptosis, improving angiogenesis, and promoting collagen synthesis and growth factor secretion. Conversely, the regenerative effects were reversed when autophagy was blocked.

Conclusions: Autophagy modulation may be a promising therapeutic strategy for improving the efficiency of tissue expansion and preventing the incidence of the complication of skin necrosis.

背景:组织扩张是一种通过机械拉伸刺激诱导皮肤再生的技术,常用于组织修复和重建。本研究旨在监测扩张刺激后扩张皮肤的自噬水平,并探讨自噬调节对皮肤再生的影响:方法:建立大鼠头皮扩张模型,以提供稳定的扩张皮肤对机械拉伸的反应。方法:建立大鼠头皮扩张模型,提供稳定的扩张皮肤对机械拉伸的反应,并在不同时间点(最后一次扩张后 6、12、24、48 和 72 h)通过 Western 印迹检测自噬水平。通过皮肤扩张效率评估、Western 印迹、免疫荧光染色、TUNEL 染色和激光多普勒血流成像评估了组织扩张期间自噬调节对皮肤再生的影响:结果:自噬通量在组织扩张 48 小时后达到最高水平。雷帕霉素激活自噬作用可增加扩张皮肤的面积以及表皮和真皮的厚度。此外,在组织扩张过程中,激活自噬可通过增强细胞增殖、表皮基底细胞和毛囊干细胞的数量、减少细胞凋亡、改善血管生成、促进胶原蛋白合成和生长因子分泌,加速皮肤再生。相反,当自噬被阻断时,再生效果就会逆转:结论:自噬调节可能是提高组织扩张效率和预防皮肤坏死并发症发生的一种有前途的治疗策略。
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引用次数: 0
Influence of scar age, laser type and laser treatment intervals on paediatric burn scars: a systematic review and meta-analysis 疤痕年龄、激光类型和激光治疗间隔对儿科烧伤疤痕的影响:系统回顾和荟萃分析
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2024-02-03 DOI: 10.1093/burnst/tkad046
Yangmyung Ma, Sabrina P Barnes, Yung-Yi Chen, Naiem Moiemen, Janet M Lord, Amanda V Sardeli
Background Laser therapy has emerged to play a valuable role in the treatment of paediatric burn scars; however, there is heterogeneity in the literature, particularly concerning optimal timing for initiation of laser therapy. This study aims to investigate the effect of factors such as scar age, type of laser and laser treatment interval on burn scar outcomes in children by meta-analysis of previous studies. Methods A literature search was conducted across seven databases in May 2022 to understand the effects of laser therapy on burn scar outcomes in paediatric patients by metanalysis of standardized mean difference (SMD) between pre- and post-laser intervention. Meta-analyses were performed using the Comprehensive Meta-Analysis software version 4.0. Fixed models were selected when there was no significant heterogeneity, and the random effects model was selected for analysis when significant heterogeneity was identified. For all analyses, a p-value &lt; 0.05 was considered significant. Results Seven studies were included in the meta-analysis with a total of 467 patients. Laser therapy significantly improved Vancouver Scar Scale (VSS)/Total Patient and Observer Scar Assessment Scale (Total POSAS), vascularity, pliability, pigmentation and scar height of burn scars. Significant heterogeneity was found between the studies and thus subgroup analyses were performed. Early laser therapy (&lt;12 months post-injury) significantly improved VSS/POSAS scores compared to latent therapy (&gt;12 months post-injury) {SMD −1.97 [95% confidence interval (CI) = −3.08; −0.87], p &lt; 0.001 vs −0.59 [95%CI = −1.10; −0.07], p = 0.03} as well as vascularity {SMD −3.95 [95%CI = −4.38; −3.53], p &lt; 0.001 vs −0.48 [95%CI = −0.66; −0.30], p &lt; 0.001}. Non-ablative laser was most effective, significantly reducing VSS/POSAS, vascularity, pliability and scar height outcomes compared to ablative, pulse dye laser and a combination of ablative and pulse dye laser. Shorter treatment intervals of &lt;4 weeks significantly reduced VSS/POSAS and scar height outcomes compared to intervals of 4 to 6 weeks. Conclusions Efficacy of laser therapy in the paediatric population is influenced by scar age, type of laser and interval between laser therapy application. The result of this study particularly challenges the currently accepted initiation time for laser treatment. Significant heterogeneity was observed within the studies, which suggests the need to explore other confounding factors influencing burn scar outcomes after laser therapy.
背景 激光疗法在治疗小儿烧伤疤痕方面发挥了重要作用;然而,文献中的研究结果却不尽相同,尤其是在开始激光治疗的最佳时机方面。本研究旨在通过对以往研究进行荟萃分析,探讨疤痕年龄、激光类型和激光治疗间隔等因素对儿童烧伤疤痕治疗效果的影响。方法 2022年5月,我们在7个数据库中进行了文献检索,通过对激光干预前后的标准化平均差(SMD)进行荟萃分析,了解激光治疗对儿童烧伤疤痕疗效的影响。荟萃分析使用 4.0 版综合荟萃分析软件进行。无明显异质性时选择固定模型,发现明显异质性时选择随机效应模型进行分析。在所有分析中,P 值为 &lt; 0.05 即为显著。结果 七项研究被纳入荟萃分析,共有 467 名患者参与。激光疗法明显改善了烧伤疤痕的温哥华疤痕量表(VSS)/患者和观察者疤痕评估总量表(Total POSAS)、血管性、柔韧性、色素沉着和疤痕高度。研究之间存在显著的异质性,因此进行了分组分析。与潜伏疗法(伤后 12 个月)相比,早期激光疗法(伤后 12 个月)能显著改善 VSS/POSAS 评分 {SMD -1.97 [95% 置信区间 (CI) = -3.08; -0.87],p&lt;0.001 vs -0.59 [95%CI = -1.10; -0.07],p = 0.03}以及血管性{SMD -3.95 [95%CI = -4.38; -3.53],p&lt;0.001 vs -0.48 [95%CI = -0.66; -0.30],p&lt;0.001}。与烧蚀、脉冲染料激光以及烧蚀和脉冲染料激光联合治疗相比,非烧蚀激光最有效,能显著降低VSS/POSAS、血管性、柔韧性和疤痕高度。与 4 至 6 周的治疗间隔相比,更短的治疗间隔(&lt;4 周)可显著降低 VSS/POSAS 和疤痕高度。结论 儿童激光治疗的疗效受疤痕年龄、激光类型和激光治疗间隔时间的影响。这项研究的结果尤其对目前公认的激光治疗开始时间提出了挑战。研究中观察到了显著的异质性,这表明有必要探索影响激光治疗后烧伤疤痕疗效的其他干扰因素。
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引用次数: 0
The cGAS-STING pathway: a therapeutic target in diabetes and its complications cGAS-STING 通路:糖尿病及其并发症的治疗靶点
IF 5.3 1区 医学 Q1 Medicine Pub Date : 2024-02-03 DOI: 10.1093/burnst/tkad050
Wenjie He, Xingrui Mu, Xingqian Wu, Ye Liu, Junyu Deng, Yiqiu Liu, Felicity Han, Xuqiang Nie
Diabetic wound healing (DWH) represents a major complication of diabetes where inflammation is a key impediment to proper healing. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway has emerged as a central mediator of inflammatory responses to cell stress and damage. However, the contribution of cGAS-STING activation to impaired healing in DWH remains understudied. In this review, we examine the evidence that cGAS-STING-driven inflammation is a critical factor underlying defective DWH. We summarize studies revealing upregulation of the cGAS-STING pathway in diabetic wounds and discuss how this exacerbates inflammation and senescence and disrupts cellular metabolism to block healing. Partial pharmaceutical inhibition of cGAS-STING has shown promise in damping inflammation and improving DWH in preclinical models. We highlight key knowledge gaps regarding cGAS-STING in DWH, including its relationships with endoplasmic reticulum stress and metal-ion signaling. Elucidating these mechanisms may unveil new therapeutic targets within the cGAS-STING pathway to improve healing outcomes in DWH. This review synthesizes current understanding of how cGAS-STING activation contributes to DWH pathology and proposes future research directions to exploit modulation of this pathway for therapeutic benefit.
糖尿病伤口愈合(DWH)是糖尿病的一种主要并发症,炎症是阻碍伤口正常愈合的关键因素。环GMP-AMP合成酶(cGAS)-干扰素基因刺激器(STING)信号通路已成为细胞应激和损伤的炎症反应的核心介质。然而,cGAS-STING 的激活对 DWH 愈合受损的影响仍未得到充分研究。在本综述中,我们研究了 cGAS-STING 驱动的炎症是导致 DWH 缺陷的关键因素的证据。我们总结了揭示糖尿病伤口中 cGAS-STING 通路上调的研究,并讨论了这是如何加剧炎症和衰老并破坏细胞代谢从而阻碍伤口愈合的。在临床前模型中,部分药物抑制 cGAS-STING 已显示出抑制炎症和改善 DWH 的前景。我们强调了有关 cGAS-STING 在 DWH 中作用的关键知识空白,包括它与内质网应激和金属离子信号转导的关系。阐明这些机制可能会在 cGAS-STING 通路中发现新的治疗靶点,从而改善 DWH 的治疗效果。本综述综述了目前对 cGAS-STING 激活如何导致 DWH 病理学的理解,并提出了未来的研究方向,以利用对该通路的调节来实现治疗效果。
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引用次数: 0
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 Medicine 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 Medicine 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 Medicine 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 Medicine 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。
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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 Medicine 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。
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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 Medicine 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。
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Burns & Trauma
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