Bibliometric analysis of the inflammatory mechanism in aortic disease.
aortic disease
inflammation
inflammatory response markers
research hotspots
Journal
Reviews in cardiovascular medicine
ISSN: 1530-6550
Titre abrégé: Rev Cardiovasc Med
Pays: Singapore
ID NLM: 100960007
Informations de publication
Date de publication:
17 Feb 2022
17 Feb 2022
Historique:
received:
14
09
2021
revised:
07
10
2021
accepted:
14
10
2021
entrez:
1
3
2022
pubmed:
2
3
2022
medline:
24
3
2022
Statut:
ppublish
Résumé
In view of the key role of inflammation in the pathogenesis of aortic disease, we visually analyzed the research hotspots of inflammatory mechanism in aortic disease in this work through the method of bibliometrics from the Web of Science (WOS) Core database over the past three decades. A visual bibliometric network of research articles on inflammatory mechanisms in aortic disease was obtained from VOSviewer and Citespace based on the WOS Core Collection. A total of 1278 documents from January 1990 to February 2021 were selected for analysis. The United States and China had the highest percentage of articles, comprising 34.01% and 24.92% of articles worldwide, respectively. Harvard University has published the most articles in this field, followed by the University of Michigan and Huazhong University of Science and Technology. The top 3 research hotspots were atherosclerosis, oxidative stress, and macrophages. The journal with the most articles in this area was Arteriosclerosis Thrombosis and Vascular Biology, followed by Atherosclerosis and PLOS One. The research trend on inflammatory mechanisms in the aortic system has 5 distinct directions: (1) atherosclerosis, NF-κB, expression, smooth muscle cell, and oxidative stress; (2) coronary artery disease, C-reactive protein, risk factors, endothelial dysfunction, and aortic stenosis; (3) abdominal aortic aneurysm, matrix metalloproteinases, macrophage, and pathogenesis; (4) cholesterol, metabolism, low-density lipoprotein, gene expression, and a therosclerotic lesions; and (5) calcific aortic valve disease, interstitial cells, calcification, and stenosis. Inflammatory mechanism research has shown a tendency to rise gradually in the aortic field. Numerous studies have explored the role of inflammatory responses in aortic disease, which may increase the risk of endothelial dysfunction (aortic fibrosis and stiffness) and induce plaque formation. Among them, NFκB activation, nitric-oxide synthase expression, and oxidative stress are particularly essential.
Sections du résumé
BACKGROUND
BACKGROUND
In view of the key role of inflammation in the pathogenesis of aortic disease, we visually analyzed the research hotspots of inflammatory mechanism in aortic disease in this work through the method of bibliometrics from the Web of Science (WOS) Core database over the past three decades.
METHODS
METHODS
A visual bibliometric network of research articles on inflammatory mechanisms in aortic disease was obtained from VOSviewer and Citespace based on the WOS Core Collection.
RESULTS
RESULTS
A total of 1278 documents from January 1990 to February 2021 were selected for analysis. The United States and China had the highest percentage of articles, comprising 34.01% and 24.92% of articles worldwide, respectively. Harvard University has published the most articles in this field, followed by the University of Michigan and Huazhong University of Science and Technology. The top 3 research hotspots were atherosclerosis, oxidative stress, and macrophages. The journal with the most articles in this area was Arteriosclerosis Thrombosis and Vascular Biology, followed by Atherosclerosis and PLOS One. The research trend on inflammatory mechanisms in the aortic system has 5 distinct directions: (1) atherosclerosis, NF-κB, expression, smooth muscle cell, and oxidative stress; (2) coronary artery disease, C-reactive protein, risk factors, endothelial dysfunction, and aortic stenosis; (3) abdominal aortic aneurysm, matrix metalloproteinases, macrophage, and pathogenesis; (4) cholesterol, metabolism, low-density lipoprotein, gene expression, and a therosclerotic lesions; and (5) calcific aortic valve disease, interstitial cells, calcification, and stenosis.
CONCLUSIONS
CONCLUSIONS
Inflammatory mechanism research has shown a tendency to rise gradually in the aortic field. Numerous studies have explored the role of inflammatory responses in aortic disease, which may increase the risk of endothelial dysfunction (aortic fibrosis and stiffness) and induce plaque formation. Among them, NFκB activation, nitric-oxide synthase expression, and oxidative stress are particularly essential.
Identifiants
pubmed: 35229558
pii: S1530-6550(22)00354-4
doi: 10.31083/j.rcm2302067
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
67Informations de copyright
© 2022 The Author(s). Published by IMR Press.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.