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TAK1 在调控细胞死亡方面的全球趋势和热点的文献计量学和可视化分析:1999 年至 2024 年。

Bibliometric and visualized analysis on global trends and hotspots of TAK1 in regulated cell death: 1999 to 2024.

机构信息

Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.

Xiangya School of Medicine, Central South University, Changsha, China.

出版信息

Front Immunol. 2024 Oct 15;15:1437570. doi: 10.3389/fimmu.2024.1437570. eCollection 2024.


DOI:10.3389/fimmu.2024.1437570
PMID:39474417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11518718/
Abstract

BACKGROUND: Regulated cell death (RCD) is a genetically controlled form of cell death that plays an important role in organogenesis, tissue remodeling, and pathogenesis of cancers. Transforming growth factor-beta-activation kinase 1 (TAK1) is a member of the serine/threonine protein kinase family, which can respond to internal and external stimuli and participate in inflammatory responses through multiple signaling pathways and cellular processes. In the last two decades, the regulatory roles of TAK1 at the crossroads of multiple RCD pathways, including apoptosis, necroptosis, pyroptosis, and PANoptosis were revealed by 801 articles retrieved from the Web of Science Core Collection database. To analyze global research trends and hotspots concerning the role of TAK1 in RCD, the bibliometric and visualized analysis were applied in the current study. METHODS: The data for this bibliometrics study were retrieved from the Web of Science Core Collection database. The search formula was (TS=(Apoptosis) OR TS=(pyroptosis) OR TS=(Necroptosis) OR TS=(PANoptosis) OR TS=(Autophagy) OR TS=(Ferroptosis) OR TS=(cuproptosis)) AND ((TS=(TAK1)) OR TS=(MAP3K7)). The co-occurrence and co-cited analysis on basic bibliometric parameters were conducted by VOSviewer. The dual-map overlay of journals, citation bursts, keyword timelines, and keyword bursts were analyzed by CiteSpace. RESULTS: A total of 801 articles from 46 countries have been included in the analysis. The number of publications demonstrates a consistent increase from 1999 to 2024. The primary research institutions driving this field are Osaka University Notably, the Journal of Biological Chemistry stands out as the most popular journal in this domain. These publications collectively involve contributions from 4663 authors, with Jun Tsuji emerging as a prolific author. Jun Tsuji also gains the highest co-citation frequency. Emerging research hotspots are encapsulated by keywords, including apoptosis, NF-κB, inflammation, autophagy, and TNFα. CONCLUSION: This is the first bibliometric and visualized study to analyze the global trends and hotspots of TAK1 in RCD. Based on the analysis of 801 articles, the results provide a retrospective and comprehensive visualized view of the research hotspots and frontiers of TAK1 at the crossroads of multiple RCD signaling pathways and propose ideas for guiding their future investigations in molecular mechanisms and therapeutic strategies in this field.

摘要

背景:细胞程序性死亡(RCD)是一种受基因调控的细胞死亡形式,在器官发生、组织重塑和癌症发病机制中发挥着重要作用。转化生长因子-β激活激酶 1(TAK1)是丝氨酸/苏氨酸蛋白激酶家族的成员,它可以通过多种信号通路和细胞过程对内外刺激做出反应,并参与炎症反应。在过去的二十年中,通过从 Web of Science Core Collection 数据库中检索到的 801 篇文章,揭示了 TAK1 在包括细胞凋亡、细胞焦亡、细胞坏死和全细胞凋亡在内的多种 RCD 途径中的调控作用。为了分析 TAK1 在 RCD 中作用的全球研究趋势和热点,本研究应用了文献计量学和可视化分析。

方法:本研究的数据来源于 Web of Science Core Collection 数据库。检索式为(TS=(Apoptosis) OR TS=(pyroptosis) OR TS=(Necroptosis) OR TS=(PANoptosis) OR TS=(Autophagy) OR TS=(Ferroptosis) OR TS=(cuproptosis))AND ((TS=(TAK1)) OR TS=(MAP3K7)。使用 Vosviewer 对基本文献计量参数的共现和共被引进行分析。通过 CiteSpace 分析期刊、引文爆发、关键词时间线和关键词爆发的双图叠加。

结果:共纳入来自 46 个国家的 801 篇文章。自 1999 年至 2024 年,出版物数量呈持续增长趋势。推动这一领域发展的主要研究机构是大阪大学。值得注意的是,《生物化学杂志》在该领域脱颖而出,成为最受欢迎的期刊。这些出版物共涉及 4663 位作者的贡献,其中 Jun Tsuji 是高产作者。Jun Tsuji 也获得了最高的共被引频次。关键词包括细胞凋亡、NF-κB、炎症、自噬和 TNFα,涵盖了新兴的研究热点。

结论:这是第一项分析 TAK1 在 RCD 中全球趋势和热点的文献计量学和可视化研究。基于对 801 篇文章的分析,结果提供了 TAK1 在多种 RCD 信号通路交汇点的研究热点和前沿的回顾性和全面的可视化视图,并为指导该领域在分子机制和治疗策略方面的未来研究提供了思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/d9aa16b72feb/fimmu-15-1437570-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/2f3dd6ea792b/fimmu-15-1437570-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/f7a59bf1dd95/fimmu-15-1437570-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/e2ed245f0d8d/fimmu-15-1437570-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/b6123ca6b555/fimmu-15-1437570-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/7299f79f79f8/fimmu-15-1437570-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/3515f37fbb57/fimmu-15-1437570-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/2a7cca202426/fimmu-15-1437570-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/4c2b9fa9fabd/fimmu-15-1437570-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/d9aa16b72feb/fimmu-15-1437570-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/2f3dd6ea792b/fimmu-15-1437570-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/f7a59bf1dd95/fimmu-15-1437570-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/e2ed245f0d8d/fimmu-15-1437570-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/b6123ca6b555/fimmu-15-1437570-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/7299f79f79f8/fimmu-15-1437570-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/3515f37fbb57/fimmu-15-1437570-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/2a7cca202426/fimmu-15-1437570-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/4c2b9fa9fabd/fimmu-15-1437570-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f72/11518718/d9aa16b72feb/fimmu-15-1437570-g009.jpg

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Front Immunol. 2025-8-4

[2]
PANoptosis in neurological disorders: mechanisms, implications, and therapeutic potential.

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[4]
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本文引用的文献

[1]
Identification of PANoptosis-related genes as prognostic indicators of thyroid cancer.

Heliyon. 2024-5-23

[2]
Identification of PANoptosis-related subtypes, construction of a prognosis signature, and tumor microenvironment landscape of hepatocellular carcinoma using bioinformatic analysis and experimental verification.

Front Immunol. 2024

[3]
PANoptosis-related genes function as efficient prognostic biomarkers in colon adenocarcinoma.

Front Endocrinol (Lausanne). 2024

[4]
Current evidence and therapeutic implication of PANoptosis in cancer.

Theranostics. 2024

[5]
Mapping the landscape of immunonutrition and cancer research: a comprehensive bibliometric analysis on behalf of NutriOnc Research Group.

Int J Surg. 2024-1-1

[6]
Immune regulator IRF1 contributes to ZBP1-, AIM2-, RIPK1-, and NLRP12-PANoptosome activation and inflammatory cell death (PANoptosis).

J Biol Chem. 2023-9

[7]
Regulated Cell Death of Retinal Ganglion Cells in Glaucoma: Molecular Insights and Therapeutic Potentials.

Cell Mol Neurobiol. 2023-10

[8]
Bibliometric analysis and mini-review of global research on pyroptosis in the field of cancer.

Apoptosis. 2023-8

[9]
DTX3L induced NLRP3 ubiquitination inhibit R28 cell pyroptosis in OGD/R injury.

Biochim Biophys Acta Mol Cell Res. 2023-3

[10]
Inhibition of mitochondrial VDAC1 oligomerization alleviates apoptosis and necroptosis of retinal neurons following OGD/R injury.

Ann Anat. 2023-4

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