ReviewFrontiers in cardiovascular medicine2024
Current research status and future prospects of NLRP3 inflammasome in cardiovascular diseases: a bibliometric and visualization analysis.
Review in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed.
- Endothelial Cell Differentiation-Related CircRNAs Drive the Differentiation of Vascular Endothelial Cells.Biochemical genetics · 2026Article
- Mapping the Inflammation Research Landscape in Myocardial Infarction, 1995-2025: A Bibliometric Analysis of WoSCC and PubMed.Journal of inflammation research · 2026Article
- The regulatory mechanism of NLRP3 inflammasome in the "immune paralytic-overactivation" imbalance in sepsis: the latest progress from molecular signaling to clinical translation.Frontiers in immunology · 2026Review
- Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cardiovascular disease (CVD) is a leading cause of global mortality, with atherosclerosis (AS) contributing to its pathological basis. Inflammation plays a critical role in the pathophysiological process of AS, and the NOD-like receptor protein 3 (NLRP3) inflammasome has been extensively studied in this context. This study aimed to analyze the research status of the NLRP3 inflammasome in cardiovascular disease and provide research directions for further exploration in this field. Methods: Using the "Bibliometrix" and "CiteSpace" software, a total of 516 articles were retrieved from the Web of Science (WoS) database published between 2012 and 2023. The search query used the keywords "["CVD" OR "cardiovascular disease"] AND ["NLRP3 inflammasome "OR "NLRP3"]". Visual analysis was performed on authors, countries, institutions, journal sources, keywords, references, and future trends. Results: A total of 516 English articles were retrieved, showing an overall upward trend in annual publication volume with slight fluctuations. China, the United States, and Europe were the countries and regions with the highest number of published articles. Among them, China had the highest article count (170), while the United States had the highest citation count (18,664), centrality score (0.43), and h-index (90), indicating its influential role in this research area. These countries also possessed elite institutions, professional researchers, and high-impact journals, making them leading contributors in this field. The main pathogenic mechanisms of the NLRP3 inflammasome in CVD were identified as "oxidative stress", "pyroptosis", and "inflammation". The most frequently studied signaling pathways included "NF-κB", "IL-1", and "C-reactive protein". The most studied disease types were coronary heart disease, atherosclerosis, metabolic syndrome, and myocardial infarction. Additionally, research on the correlation between cholesterol markers and inflammatory indicators associated with NLRP3 inflammasome in CVD risk assessment has gained significant momentum, with the main mechanism being NLRP3/IL-6/hs-CRP and cholesterol lipoproteins emerging as a major keyword in this context. Conclusion: This study provides valuable insights into the research hotspots and emerging trends of the NLRP3 inflammasome in cardiovascular disease. The findings offer guidance for researchers and scholars in this field and facilitate the exploration of new research directions.
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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.