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Comparing Bibliometric Analysis Using PubMed, Scopus, and Web of Science Databases
Published on: October 24, 2019
A bibliometric analysis of autophagy research in atherosclerosis over the past decade
Wen-Qing Xu1, Ying-Xi Yang2, Yue Ma3
1Heart Center, Guilin People's Hospital, Guangxi, China.
Insights
Autophagy plays a key role in atherosclerosis, impacting vascular cells and plaque stability. Understanding its mechanisms offers new therapeutic targets for cardiovascular disease prevention and treatment.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Biomedical Science
Background:
- Atherosclerosis (AS) is a major risk factor for cardiovascular diseases, involving dyslipidemia, thrombosis, and inflammation.
- Autophagy, a cellular process for degrading damaged components, is critical in maintaining homeostasis.
- Autophagy's role in AS pathogenesis, particularly in endothelial cells, macrophages, and VSMCs, affects inflammation and lipid metabolism, but mechanisms are complex.
Purpose of the Study:
- To analyze the research landscape of autophagy in atherosclerosis from 2014-2024.
- To identify publication trends, key contributors, and research hotspots in this field.
- To provide insights for future research directions in autophagy and atherosclerosis.
Main Methods:
- Bibliometric analysis using CiteSpace and R-Bibliometrix tools.
- Examination of publication trends, country/institution contributions, and journal distribution.
- Analysis of keyword co-occurrence and co-citation networks.
Main Results:
- Significant growth in research on autophagy in atherosclerosis, accelerating recently.
- Research focuses on autophagy's role in vascular cells (endothelial cells, macrophages, VSMCs), inflammation, oxidative stress, and lipid metabolism.
- Moderate autophagy supports vascular cell survival and plaque stability; excessive autophagy may promote cell death and AS progression.
Conclusions:
- Autophagy is crucial for mitochondrial quality control and mitigating plaque formation in AS.
- Elucidating autophagy's regulatory mechanisms in vascular cells can reveal novel therapeutic targets for AS.
- Bibliometric analysis highlights research trends, guiding future investigations in autophagy and atherosclerosis.
Background:
Atherosclerosis (AS) is a critical risk factor in the development of cardiovascular diseases, primarily characterized by dyslipidemia, thrombosis, and inflammatory responses, significantly impairing patients' quality of life. Autophagy, one of the fundamental cellular processes, plays a pivotal role in maintaining cellular homeostasis by degrading damaged organelles and macromolecules. In the pathogenesis and progression of atherosclerosis, autophagy is crucial, particularly in the regulation of endothelial cells, macrophages, and vascular smooth muscle cells (VSMCs), affecting various processes such as inflammation and lipid metabolism. However, the underlying mechanisms of autophagy in atherosclerosis remain complex and require further elucidation.
Methods:
This study employed CiteSpace and R-Bibliometrix, bibliometric tools, to conduct a visualized analysis of the literature on autophagy in atherosclerosis from 2014 to 2024. Key aspects such as publication trends, research contributions from different countries/institutions, journal distribution, and keyword co-occurrence and co-citation relationships were thoroughly examined.
Results:
The analysis revealed a rapid growth in research on autophagy in atherosclerosis, with a marked acceleration in recent years. The focus of the research predominantly centered on the role of autophagy in endothelial cells, macrophages, and VSMCs, as well as its involvement in inflammation, oxidative stress, and lipid metabolism. Moderate autophagy contributes to the survival of vascular cells and the stabilization of atherosclerotic plaques, while excessive autophagy may lead to programmed cell death, exacerbate inflammation, and accelerate the progression of AS.
Conclusion:
The significance of autophagy in atherosclerosis has garnered extensive attention, particularly its role in maintaining mitochondrial quality and mitigating plaque formation. A deeper understanding of the regulatory mechanisms of autophagy, especially in vascular cells, could provide novel targets and strategies for the prevention and treatment of atherosclerosis. Bibliometric analysis further highlights the research hotspots and trends in the field, offering valuable insights and guidance for future studies.
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