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NLRP3 Inflammasome and IL-1–Mediated Inflammation in Human Carotid Atherosclerosis

2026-06Recensão Acesso aberto
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dc.contributor.authorMendonça-Soares, David
dc.contributor.authorRocha-Melo-Sousa, Antónia
dc.contributor.authorShahat, Mohammed
dc.contributor.authorTavares, Cármen
dc.contributor.authorCarvalho, Lina
dc.contributor.authorSá-Martins, Vitor
dc.contributor.authorNeiva-Sousa, Manuel
dc.contributor.authorFragão-Marques, Mariana
dc.contributor.authorNeves, João Rocha
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2026-07-14T14:23:01Z
dc.date.available2026-07-14T14:23:01Z
dc.date.issued2026-06
dc.descriptionPublisher Copyright: © 2026 by the authors.
dc.description.abstractBackground: Carotid atherosclerosis and plaque instability are major drivers of ischemic stroke. The NLRP3 inflammasome and interleukin-1 (IL-1) pathway are recognized as key upstream regulators of atherogenesis. This systematic review aims to synthesize the available evidence regarding the impact of NLRP3 and IL-1-mediated inflammation on plaque vulnerability and clinical outcomes in patients undergoing carotid endarterectomy (CEA). Materials and Methods: A systematic search was performed relying on MEDLINE, Scopus, and Web of Science for studies assessing NLRP3 inflammasome and IL-1-mediated biomarkers in adult patients undergoing CEA. Data extraction and risk-of-bias evaluation were independently performed using the National Heart, Lung, and Blood Institute (NHLBI) Quality Assessment Tool. Due to substantial methodological heterogeneity, a narrative synthesis was conducted. Results: Sixteen studies involving 1677 participants were included. Evidence demonstrates that NLRP3 inflammasome components (NLRP3, ASC, Caspase-1) and IL-1 family cytokines (IL-1β, IL-18) are consistently elevated in unstable plaques and in symptomatic patients compared to asymptomatic counterparts. These markers were associated with histological features of instability, such as intraplaque haemorrhage, large lipid cores and extensive macrophage infiltration. While some data suggest a link between these biomarkers and Major Adverse Cardiovascular Events (MACE), most studies were limited by a lack of adjusted multivariable modelling and an overall unclear risk of bias. Conclusions: NLRP3/IL-1/-mediated inflammation is a promising biomarker axis for carotid plaque vulnerability and symptomatic disease. However, small, heterogeneous cohorts and limited adjusted analyses highlight the need for larger, well-designed studies to refine risk stratification and guide targeted anti-inflammatory strategies in carotid atherosclerosis.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1340072
dc.identifier.doi10.3390/medsci14020280
dc.identifier.issn2076-3271
dc.identifier.otherPURE: 167697110
dc.identifier.otherPURE UUID: af32eb23-d49e-474a-953c-da31555d816e
dc.identifier.otherScopus: 105042799123
dc.identifier.otherPubMed: 42346819
dc.identifier.urihttp://hdl.handle.net/10362/204509
dc.identifier.urlhttps://www.scopus.com/pages/publications/105042799123
dc.language.isoeng
dc.peerreviewedyes
dc.subjectatherosclerosis
dc.subjectbiomarkers
dc.subjectcarotid artery diseases
dc.subjectcytokines
dc.subjectprognosis
dc.subjectrisk factors
dc.subjectGeneral Medicine
dc.titleNLRP3 Inflammasome and IL-1–Mediated Inflammation in Human Carotid Atherosclerosisen
dc.title.subtitleA Systematic Review of Endarterectomy-Based Evidenceen
dc.typereview
degois.publication.issue2
degois.publication.titleMedical sciences
degois.publication.volume14
dspace.entity.typePublication
rcaap.rightsopenAccess

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