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氧化应激与心肌纤维化的全球研究趋势：一项双软件文献计量学研究

Global Research Trends in Oxidative Stress and Myocardial Fibrosis: A Dual-Software Bibliometric Study.

作者信息

Jia Sihan, Lian Yanjie, Lai Xiaolei, Li Sinai, Shang Juju, Liu Hongxu

机构信息

Department of Cardiovascular, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, 100010, People's Republic of China.

Beijing Institute of Traditional Chinese Medicine, Beijing, 100010, People's Republic of China.

出版信息

J Multidiscip Healthc. 2025 Jun 11;18:3357-3372. doi: 10.2147/JMDH.S525389. eCollection 2025.

DOI:10.2147/JMDH.S525389
PMID:40524731
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12168942/
Abstract

OBJECTIVE: To conduct a visualization analysis of the literature on the role of oxidative stress in myocardial fibrosis (MF), explore the research progress, frontier hotspots, and development trends in this field, with the aim of providing a reference for the research on the prevention and treatment of MF related to oxidative stress. METHODS: Web of Science was selected as the data source, and the relevant English literature on the role of oxidative stress in MF from the database establishment to December 31, 2024 was collected. Bibliometric methods were used for statistical analysis of the literature that met the research standards, and CiteSpace 6.3.R2 and VOSviewer 1.6.20 software were used for visualization of information such as publishing countries, institutions, authors, and keywords. RESULTS: A total of 1831 SCI articles were included. The global publication volume showed an upward trend year by year, Publications increased by 16% annually after 2014, with China and the United States leading in publication volume. Keyword and cited literature analysis showed that the research hotspots and frontiers in this field mainly include the phenomenon of extracellular matrix (ECM) cell migration, the activation of the renin-angiotensin-aldosterone system, the regulatory mechanisms of oxidative stress in MF of different etiologies, and the mechanisms of action of oxidative stress in MF. CONCLUSION: The field of research into the role of oxidative stress in myocardial fibrosis is currently experiencing a period of rapid expansion. By leveraging the complementary strengths of CiteSpace for analyzing temporal and geographic trends, and VOSviewer for mapping collaboration networks, researchers have gained multidimensional insights into this area. The identification of the NLRP3 inflammasome as the fastest-growing research frontier, highlights its potential as a novel therapeutic target for clinical investigation. The mechanism by which oxidative stress activates the NLRP3 inflammasome signaling pathway to promote myocardial fibrosis is likely to emerge as a significant future research trend and warrants further in-depth exploration and study.

摘要

目的：对氧化应激在心肌纤维化（MF）中作用的文献进行可视化分析，探究该领域的研究进展、前沿热点及发展趋势，为氧化应激相关MF防治研究提供参考。 方法：选取Web of Science作为数据源，收集数据库建立至2024年12月31日关于氧化应激在MF中作用的相关英文文献。采用文献计量学方法对符合研究标准的文献进行统计分析，运用CiteSpace 6.3.R2和VOSviewer 1.6.20软件对发表国家、机构、作者及关键词等信息进行可视化。 结果：共纳入1831篇SCI论文。全球发文量呈逐年上升趋势，2014年后每年增长16%，中国和美国发文量领先。关键词及被引文献分析表明，该领域研究热点和前沿主要包括细胞外基质（ECM）细胞迁移现象、肾素 - 血管紧张素 - 醛固酮系统激活、不同病因MF中氧化应激的调控机制以及氧化应激在MF中的作用机制。 结论：氧化应激在心肌纤维化中作用的研究领域目前正处于快速发展阶段。通过利用CiteSpace分析时间和地理趋势的互补优势以及VOSviewer绘制合作网络，研究人员对该领域有了多维度的见解。将NLRP3炎性小体确定为增长最快的研究前沿，凸显了其作为临床研究新治疗靶点的潜力。氧化应激激活NLRP3炎性小体信号通路促进心肌纤维化的机制可能成为未来重要的研究趋势，值得进一步深入探索和研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a27e/12168942/c98bbe9328db/JMDH-18-3357-g0009.jpg
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Global Research Trends in Oxidative Stress and Myocardial Fibrosis: A Dual-Software Bibliometric Study.

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本文引用的文献

[1]
Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.

ESC Heart Fail. 2025-4

[2]
2-APQC, a small-molecule activator of Sirtuin-3 (SIRT3), alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis.

Signal Transduct Target Ther. 2024-5-15

[3]
Possible Role of Gut Microbiota Alterations in Myocardial Fibrosis and Burden of Heart Failure in Hypertensive Heart Disease.

Hypertension. 2024-7

[4]
The Roles of Exosome-Derived microRNAs in Cardiac Fibrosis.

Molecules. 2024-3-7

[5]
Targeting MAPK-ERK/JNK pathway: A potential intervention mechanism of myocardial fibrosis in heart failure.

Biomed Pharmacother. 2024-4

[6]
Current experimental and early investigational agents for cardiac fibrosis: where are we at?

Expert Opin Investig Drugs. 2024-4

[7]
NLRP3 inflammasome activation and symptom burden in KRAS-mutated CMML patients is reverted by IL-1 blocking therapy.

Cell Rep Med. 2023-12-19

[8]
Obesity Enables NLRP3 Activation and Induces Myocardial Fibrosis via Hyperacetylation of HADHa.

Diabetes. 2023-11-1

[9]
Interleukin-34-NF-κB signaling aggravates myocardial ischemic/reperfusion injury by facilitating macrophage recruitment and polarization.

EBioMedicine. 2023-9

[10]
CAR T therapy beyond cancer: the evolution of a living drug.

Nature. 2023-7

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