ReviewInflammation2023
NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation.
Review in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 26 citations in OpenAlex.
- Luteolin ameliorates sympathetic stress-induced myocardial injury by inhibiting the VEGFA/VEGFR2 and PI3K/Akt/NF-kappaB signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- IGF2BP1 modulates ZDHHC5-mediated NLRP3 inflammasome activation to promote mitochondrial damage and foam cell formation of vascular smooth muscle cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Bibliometric analysis of research trends on nanotechnology applications in atherosclerosis.Discover nano · 2026Review
- A bibliometric analysis of autophagy research in atherosclerosis over the past decade.Medicine · 2026Review
- Resmetirom attenuates atherosclerosis-associated dyslipidemia and vascular inflammation in high-fat diet-fed ApoE-/- mice.PloS one · 2026Article
- Review
- Effects of Mytilus edulis derived plasmalogens against atherosclerosis via lipid metabolism and MAPK signaling pathway.NPJ science of food · 2025Article
- Discovery of (Molecules (Basel, Switzerland) · 2025Article
- Bioinformatics analysis and experimental validation of potential targets and pathways in chronic kidney disease associated with renal fibrosis.Journal of translational medicine · 2025Article
- Targeting the NLRP3 inflammasome as a novel therapeutic target for osteoarthritis.Inflammopharmacology · 2025Review
- Review
- Role of Gut Microbial Metabolites in Cardiovascular Diseases-Current Insights and the Road Ahead.International journal of molecular sciences · 2024Review
- Chlojaponilactone B Attenuates THP-1 Macrophage Pyroptosis by Inhibiting the TLR/MyD88/NF-κB Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Melatonin stabilizes atherosclerotic plaques: an association that should be clinically exploited.Frontiers in medicine · 2024Review
- Pharmacological mechanisms by which baicalin ameliorates cardiovascular disease.Frontiers in pharmacology · 2024Review
- Deacetylation of Histones and Non-histone Proteins in Inflammatory Diseases and Cancer Therapeutic Potential of Histone Deacetylase Inhibitors.Current genomics · 2023Review
- Oridonin attenuates the progression of atherosclerosis by inhibiting NLRP3 and activating Nrf2 in apolipoprotein E-deficient mice.Inflammopharmacology · 2023Article
- Ononin alleviates DSS-induced colitis through inhibiting NLRP3 inflammasome via triggering mitophagy.Immunity, inflammation and disease · 2023Article
- Inflammatory Response: A Crucial Way for Gut Microbes to Regulate Cardiovascular Diseases.Nutrients · 2023Review
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is a chronic inflammatory disease with thickening or hardening of the arteries, which led to the built-up of plaques in the inner lining of an artery. Among all the clarified pathogenesis, the over-activation of inflammatory reaction is one of the most acknowledged one. The nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3 (NLRP3) inflammasome, as a vital and special form of inflammation and innate immunity, has been widely revealed to participate in the onset and development of AS. This review will introduce the process of the pathogenesis and progression of AS, and will describe the biological features of the NLRP3 inflammasome. Furthermore, the role of the NLRP3 inflammasome in AS and the possible mechanisms will be discussed. In addition, several kinds of agents with the effect of anti-atherosclerotic taking advantage of the NLRP3 inflammasome intervention will be described and discussed in detail, including natural compounds (baicalin, dihydromyricetin, luteolin, 5-deoxy-rutaecarpine (R3) and Salvianolic acid A, etc.), microRNAs (microRNA-30c-5p, microRNA-9, microRNA-146a-5p, microRNA-16-5p and microRNA-181a, etc.), and autophagy regulators (melatonin, dietary PUFA and arglabin, etc.). We aim to provide novel insights in the exploration of the specific mechanisms of AS and the development of new treatments of AS.
Indexed as
Identifiers
What OpenQuestion holds
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.