ReviewMedicine2026
A bibliometric analysis of autophagy research in atherosclerosis over the past decade.
Review in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis (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.
methodsThis 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.
resultsThe 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.
conclusionThe 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.