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线粒体损伤对肿瘤微环境和免疫反应的影响:全面的文献计量学分析。

Impact of mitochondrial damage on tumor microenvironment and immune response: a comprehensive bibliometric analysis.

机构信息

Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China.

Department of Urology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China.

出版信息

Front Immunol. 2024 Jul 22;15:1442027. doi: 10.3389/fimmu.2024.1442027. eCollection 2024.

DOI:10.3389/fimmu.2024.1442027
PMID:39104527
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11298338/
Abstract

BACKGROUND

Mitochondrial damage contributes to apoptosis, oxidative stress, and inflammation, which collectively impact the immune system's function and the tumor microenvironment (TME). These processes, in turn, influence tumor cell growth, migration, and response to treatment.

OBJECTIVE

We conducted a bibliometric analysis to elucidate the complex interactions between mitochondrial damage, the immune system, and the TME.

METHODS

Data were sourced from the Science Citation Index Core Collection (WoSCC) and analyzed using advanced tools like VOSviewer and Citespace. Our focus was on literature published between 1999 and 2023 concerning the interactions between mitochondrial damage and the TME, as well as immune responses to tumors. The analysis included regional contributions, journal influence, institutional collaborations, authorship, co-cited authors, and keyword citation bursts.

RESULTS

Our research encompassed 2,039 publications, revealing an increasing trend in annual output exploring the relationship between mitochondrial damage, TME dynamics, and immune responses. China, the United States, and South Korea emerged as the leading contributors. Prominent institutions included Institut National de la Santé et de la Recherche Médicale, University of Texas System, China Medical University, and Sun Yat-sen University. Key journals in this field are the International Journal of Molecular Sciences, Mitochondrion, and the European Journal of Pharmacology. Liang H and Wallace DC were identified as the most productive and co-cited authors, respectively. Keyword analysis highlighted the critical roles of inflammatory responses, oxidative stress, and the immune system in recent research.

CONCLUSION

This bibliometric analysis provides a comprehensive overview of historical and current research trends, underscoring the pivotal role of mitochondrial damage in the TME and immune system.

摘要

背景

线粒体损伤会导致细胞凋亡、氧化应激和炎症,这些共同作用会影响免疫系统的功能和肿瘤微环境(TME)。这些过程反过来又会影响肿瘤细胞的生长、迁移和对治疗的反应。

目的

我们进行了文献计量学分析,以阐明线粒体损伤、免疫系统和 TME 之间的复杂相互作用。

方法

数据来自科学引文索引核心集(WoSCC),并使用 VOSviewer 和 Citespace 等高级工具进行分析。我们的重点是研究 1999 年至 2023 年期间发表的关于线粒体损伤与 TME 以及肿瘤免疫反应之间相互作用的文献。该分析包括区域贡献、期刊影响力、机构合作、作者、共同引用作者和关键词引文爆发。

结果

我们的研究涵盖了 2039 篇出版物,揭示了年度产出呈上升趋势,探索了线粒体损伤、TME 动态和免疫反应之间的关系。中国、美国和韩国是主要贡献者。主要机构包括法国国家健康与医学研究所、德克萨斯大学系统、中国医科大学和中山大学。该领域的主要期刊是《国际分子科学杂志》、《线粒体》和《欧洲药理学杂志》。梁和 Wallace DC 分别被确定为最有生产力和共同引用的作者。关键词分析强调了炎症反应、氧化应激和免疫系统在最近研究中的关键作用。

结论

这项文献计量学分析提供了对历史和当前研究趋势的全面概述,强调了线粒体损伤在 TME 和免疫系统中的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/8d91a238982e/fimmu-15-1442027-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/5a6b52b3ccc2/fimmu-15-1442027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/28117f5f56dd/fimmu-15-1442027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/3c3854f5586c/fimmu-15-1442027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/2721819c2518/fimmu-15-1442027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/d3d664f70942/fimmu-15-1442027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/c37288de5a24/fimmu-15-1442027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/d3a4194ff02d/fimmu-15-1442027-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/8d91a238982e/fimmu-15-1442027-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/5a6b52b3ccc2/fimmu-15-1442027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/28117f5f56dd/fimmu-15-1442027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/3c3854f5586c/fimmu-15-1442027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/2721819c2518/fimmu-15-1442027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/d3d664f70942/fimmu-15-1442027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/c37288de5a24/fimmu-15-1442027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/d3a4194ff02d/fimmu-15-1442027-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c250/11298338/8d91a238982e/fimmu-15-1442027-g008.jpg

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