Show simple item record

dc.contributor.authorAltara, Raffaele
dc.contributor.authorGhali, Rana
dc.contributor.authorMallat, Ziad
dc.contributor.authorCataliotti, Alessandro
dc.contributor.authorBooz, George W
dc.contributor.authorZouein, Fouad A
dc.date.accessioned2018-10-03T04:44:00Z
dc.date.available2018-10-03T04:44:00Z
dc.date.issued2018-10-01
dc.identifier.issn0008-6363
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/283043
dc.description.abstractInterleukin 33 (IL-33), which is expressed by several immune cell types, endothelial and epithelial cells, and fibroblasts, is a cytokine of the IL-1 family that acts both intra- and extracellularly to either enhance or resolve the inflammatory response. Intracellular IL-33 acts in the nucleus as a regulator of transcription. Once released from cells by mechanical stress, inflammatory cytokines, or necrosis, extracellular IL-33 is proteolytically processed to act in an autocrine/paracrine manner as an 'alarmin' on neighbouring or various immune cells expressing the ST2 receptor. Thus, IL-33 may serve an important role in tissue preservation and repair in response to injury; however, the actions of IL-33 are dampened by a soluble form of ST2 (sST2) that acts as a decoy receptor and is produced by endothelial and certain immune cells. Accumulating evidence supports the conclusion that sST2 is a biomarker of vascular health with diagnostic and/or prognostic value in various cardiovascular diseases, including coronary artery disease, myocardial infarction, atherosclerosis, giant-cell arteritis, acute aortic dissection, and ischaemic stroke, as well as obesity and diabetes. Although sST2 levels are positively associated with cardiovascular disease severity, the assumption that IL-33 is always beneficial is naïve. It is increasingly appreciated that the pathophysiological importance of IL-33 is highly dependent on cellular and temporal expression. Although IL-33 is atheroprotective and may prevent obesity and type 2 diabetes by regulating lipid metabolism, IL-33 appears to drive endothelial inflammation. Here, we review the current knowledge of the IL-33/ST2/sST2 signalling network and discuss its pathophysiological and translational implications in cardiovascular diseases.
dc.format.mediumPrint
dc.languageeng
dc.publisherOxford University Press (OUP)
dc.subjectEndothelial Cells
dc.subjectImmune System
dc.subjectAnimals
dc.subjectHumans
dc.subjectCardiovascular Diseases
dc.subjectDiabetes Mellitus, Type 2
dc.subjectObesity
dc.subjectInflammation
dc.subjectInflammation Mediators
dc.subjectCell Communication
dc.subjectSignal Transduction
dc.subjectLipid Metabolism
dc.subjectBiomarkers
dc.subjectInterleukin-33
dc.subjectInterleukin-1 Receptor-Like 1 Protein
dc.titleConflicting vascular and metabolic impact of the IL-33/sST2 axis.
dc.typeArticle
prism.endingPage1594
prism.issueIdentifier12
prism.publicationDate2018
prism.publicationNameCardiovasc Res
prism.startingPage1578
prism.volume114
dc.identifier.doi10.17863/CAM.30406
dcterms.dateAccepted2018-06-28
rioxxterms.versionofrecord10.1093/cvr/cvy166
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-10
dc.contributor.orcidMallat, Ziad [0000-0003-0443-7878]
dc.identifier.eissn1755-3245
rioxxterms.typeJournal Article/Review
pubs.funder-project-idBritish Heart Foundation (RG/15/11/31593)
pubs.funder-project-idBritish Heart Foundation (PG/15/99/31865)
cam.issuedOnline2018-07-02
rioxxterms.freetoread.startdate2019-10-31


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record