Key result
Atherosclerosis autophagy research expands rapidly over ~10 years, concentrating on endothelial, macrophage, and smooth muscle cells.
This bibliometric analysis highlights the rapid growth and key research hotspots regarding the role of autophagy in atherosclerosis, particularly its effects on vascular cells and plaque stabilization.
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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Xu et al. (2026) conducted a review in Atherosclerosis. Autophagy research literature was evaluated on Publication trends, research contributions, journal distribution, and keyword co-occurrence. Bibliometric analysis from 2014 to 2024 revealed a rapid growth in research on autophagy in atherosclerosis, focusing predominantly on endothelial cells, macrophages, and vascular smooth muscle cells.
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