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Macrophage-driven inflammation in acute kidney injury: Therapeutic opportunities and challenges
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-13 DOI: 10.1016/j.trsl.2025.02.003
Ya-Fan Mu , Zi-Hui Mao , Shao-Kang Pan , Dong-Wei Liu , Zhang-Suo Liu , Peng Wu , Zhong-Xiuzi Gao
Acute kidney injury (AKI) is increasingly being recognized as a systemic disorder associated with significant morbidity and mortality. AKI manifests with extensive cellular damage, necrosis, and an intense inflammatory response, often leading to late-stage interstitial fibrosis. Although the mechanisms underlying renal injury and repair remain poorly understood, macrophages (pivotal inflammatory cells) play central roles in AKI. They undergo polarization into pro-inflammatory and anti-inflammatory phenotypes, contributing dynamically to both the injury and repair processes while maintaining homeostasis. Macrophages modulate microenvironmental inflammation by releasing extracellular vesicles (EVs) containing pro- or anti-inflammatory signaling molecules, thereby influencing the regulation of tissue injury. The injured tissue cells release EVs and activate local macrophages to initiate these responses. Our bibliometric analysis indicated that a shift has occurred in AKI macrophage research towards therapeutic strategies and clinical translation, focusing on macrophage-targeted therapies, including exosomes and nanoparticles. This review highlights the roles and mechanisms of macrophage activation, phenotypic polarization, and trans-differentiation in AKI and discusses macrophage-based approaches for AKI prevention and treatment. Understanding the involvement of macrophages in AKI contributes to the comprehension of related immune mechanisms and lays the groundwork for novel diagnostic and therapeutic avenues.
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引用次数: 0
Multi-Omics Analysis Links Mitochondrial-Related Genes to Idiopathic Pulmonary Fibrosis and In Vivo Transcriptome Validation
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-12 DOI: 10.1016/j.trsl.2025.02.002
Xiaoxia Li , Qiaojing Lin , Bingyue Guan , Minghuan Yang , Xingxin Huang , Lianhuang Li , Chun Chen , Jinsheng Hong , Mingwei Zhang
Mitochondrial dysfunction is closely associated with idiopathic pulmonary fibrosis (IPF). However, the causal association between mitochondria-related genes and IPF remains to be determined. We obtained gene expression, protein abundance, and methylation quantitative trait locus data for mitochondria-related genes from previous studies. Genome-wide association study data for patients with IPF were obtained from the FinnGen study. A two-sample Mendelian randomisation analysis was conducted to assess the association between mitochondria-related genes and IPF. Furthermore, we conducted validation of expression differences utilizing transcriptome data derived from the BLM-induced pulmonary fibrosis mouse model (n=15). Concurrently, multiphoton imaging was utilized to quantify collagen contents and structural assessment. The direction of causality was verified using the Steiger test, and colocalisation analysis was used to better validate causality. Single-cell data were used to explore the localisation and expression of positive genes across different cell types. The study identified significant associations between mitochondria-related genes and IPF, with POLG and NDUFB10 classified as Grade 1; LYRM4, NBR1, and ACSF3 as Grade 2; MCL1, GFER, MFN2, IVD, and SLC25A35 as Grade 3; and METAP1D and MTX1 as Grade 4. Single-cell analysis showed elevated expression of NBR1, MCL1, and MTX1 in pulmonary myofibroblasts of IPF. This study elucidated the causal effects of mitochondria-related genes on IPF, underscoring their significance in pathogenesis. These findings contribute to an improved understanding of the mechanisms underlying IPF, offering new potential therapeutic targets for interventions.
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引用次数: 0
Author Guidelines
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00017-9
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引用次数: 0
Information for Readers
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00018-0
{"title":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(25)00018-0","DOIUrl":"10.1016/S1931-5244(25)00018-0","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"277 ","pages":"Page IBC"},"PeriodicalIF":6.4,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143378281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Editorial Advisory Board
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-11 DOI: 10.1016/S1931-5244(25)00016-7
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引用次数: 0
Corrigendum to “Early vascular aging in chronic kidney disease: focus on microvascular maintenance, senescence signature and potential therapeutics” [Translational Research 275 (2025) 32–47] “慢性肾脏疾病的早期血管衰老:关注微血管维持、衰老特征和潜在治疗方法”[Translational Research] 275(2025) 32-47]。
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.003
Samsul Arefin , Neja Mudrovcic , Sam Hobson , Federico Pietrocola , Thomas Ebert , Liam J. Ward , Anna Witasp , Leah Hernandez , Lars Wennberg , Torbjörn Lundgren , Julia Steinmetz-Späh , Karin Larsson , Anders Thorell , Stefania Bruno , Marita Marengo , Vincenzo Cantaluppi , Peter Stenvinkel , Karolina Kublickiene
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引用次数: 0
Infectious agents in the pathogenesis of autoimmune rheumatic diseases 自身免疫性风湿病发病机制中的传染因子。
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.004
Aleksandra Korzeniowska, Ewa Bryl
Autoimmune rheumatic diseases (AIRDs) are diseases with complex outset and courses, in which both genetic and environmental factors participate. Many environmental factors can be committed to AIRDs outset and development. The most popular of them, with confirmed impact, are smoking, age, gender, and microorganisms. In light of recent research an assumption about the importance of various microorganisms in the pathogenesis of AIRDs is growing in popularity.
The human immune system has various protective mechanisms against infectious antigens which in normal cases let organism manage potential infection faster and more effectively. Unfortunately in some situations, specific errors in those mechanisms can cause an autoreactive response despite mitigation of infection. Viruses including EBV, CMV, and even SARS-CoV2 can cause these errors. This in combination with genetic factors can lead to rheumatic disease development.
This research aims to provide a brief review of the role of viruses in the outset and development of AIRDs.
自身免疫性风湿病(AIRDs)是一种发病和病程复杂的疾病,遗传和环境因素都参与其中。许多环境因素可以对aird的开始和发展作出承诺。其中最受欢迎的是吸烟、年龄、性别和微生物。根据最近的研究,关于各种微生物在AIRDs发病机制中的重要性的假设越来越受欢迎。人体免疫系统对感染性抗原有多种保护机制,在正常情况下,这些机制使生物体更快、更有效地控制潜在的感染。不幸的是,在某些情况下,这些机制中的特定错误可能导致自身反应性反应,尽管感染减轻了。包括EBV、CMV甚至SARS-CoV2在内的病毒都可能导致这些错误。这与遗传因素相结合可导致风湿病的发展。本研究旨在简要回顾病毒在AIRDs发病和发展中的作用。
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引用次数: 0
Dissecting the cellular reprogramming and tumor microenvironment in left- and right-sided Colorectal Cancer by single cell RNA sequencing 通过单细胞 RNA 测序剖析左右侧结直肠癌的细胞重编程和肿瘤微环境
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.002
Congxue Hu, Xiaozhi Huang, Jing Chen, Weixin Liang, Kaiyue Yang, Hui Jiang, Kuan Yang, Qi Ou, Xia Li, Yunpeng Zhang
Sidedness and staging are major sources of tumor microenvironment (TME) differences in colorectal cancer (CRC). Subpopulation compositions of stromal cells and immune cells, and interactions between cells collectively constitute the immunosuppressive microenvironment of CRC. In this study, we comprehensively collected single-cell RNA sequencing data from public databases. We filtered out 126,279 cells from 55 CRC samples to characterize the differences in cellular composition, and to elucidate the transcriptional features and potential functions of cell types, temporally and positionally. We observed an increased degree of hypoxia in right side-specific cancer cells compared to left-sided cancer. Cancer-associated fibroblasts (CAFs) illustrated molecular signatures tremendously tended to be associated with functions that orchestrate extracellular matrix remodeling and angiogenesis, and right-sided CAFs characterized the stronger cancer invasion signals. Crosstalk between side-specific cancer cells and stromal together with immune cells characterized CRC via different sample groups, and was pertinent to worse prognosis. Our study captured immunosuppressive pattern exhibiting more intricate intercellular interactions in right-sided CRC. Additionally, during malignant progression of CRC, the transformation of CD8+ T cell cytotoxic and exhausted properties and macrophage pro-inflammatory and anti-inflammatory properties epitomized the cellular reprogramming phenomenon that the function of TME shifted from promoting immunity to suppressive immunity. Our study shed lights on refining personalized therapeutic regimens during malignant progression in left- and right-sided CRCs.
分侧和分期是结直肠癌(CRC)肿瘤微环境(TME)差异的主要来源。基质细胞和免疫细胞的亚群组成以及细胞间的相互作用共同构成了 CRC 的免疫抑制微环境。在这项研究中,我们从公共数据库中全面收集了单细胞 RNA 测序数据。我们从 55 个 CRC 样本中筛选出 126,279 个细胞,以描述细胞组成的差异,并从时间和位置上阐明细胞类型的转录特征和潜在功能。与左侧癌细胞相比,我们观察到右侧特异性癌细胞的缺氧程度有所增加。癌症相关成纤维细胞(CAFs)的分子特征表明,它们与协调细胞外基质重塑和血管生成的功能密切相关,而右侧的CAFs具有更强的癌症侵袭信号特征。侧特异性癌细胞与基质细胞和免疫细胞之间的串扰是不同样本组 CRC 的特征,并与较差的预后有关。我们的研究捕捉到的免疫抑制模式在右侧 CRC 中表现出更复杂的细胞间相互作用。此外,在 CRC 恶性发展过程中,CD8+ T 细胞的细胞毒性和耗竭特性以及巨噬细胞的促炎和抗炎特性的转变,都是细胞重编程现象的缩影,即 TME 的功能从促进免疫转变为抑制免疫。我们的研究为完善左右侧 CRC 恶性进展过程中的个性化治疗方案提供了启示。
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引用次数: 0
Corrigendum to “Tumor molecular landscape of Epstein-Barr virus (EBV) related nasopharyngeal carcinoma in EBV-endemic and non-endemic areas: Implications for improving treatment modalities” [Transl. Res. 265 (2024) 1-16] eb病毒(EBV)相关鼻咽癌在eb病毒流行地区和非流行地区的肿瘤分子格局:改善治疗方式的意义[译]。Res. 265(2024) 1-16]。
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.trsl.2024.12.001
Deborah Lenoci , Carlo Resteghini , Mara S. Serafini , Federico Pistore , Silvana Canevari , Brigette Ma , Stefano Cavalieri , Salvatore Alfieri , Annalisa Trama , Lisa Licitra , Loris De Cecco
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引用次数: 0
Author Guidelines
IF 6.4 2区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/S1931-5244(25)00005-2
{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(25)00005-2","DOIUrl":"10.1016/S1931-5244(25)00005-2","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"276 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
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Translational Research
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