Conflicting vascular and metabolic impact of the IL-33/sST2 axis.
dc.contributor.author | Altara, Raffaele | |
dc.contributor.author | Ghali, Rana | |
dc.contributor.author | Mallat, Ziad | |
dc.contributor.author | Cataliotti, Alessandro | |
dc.contributor.author | Booz, George W | |
dc.contributor.author | Zouein, Fouad A | |
dc.date.accessioned | 2018-10-03T04:44:00Z | |
dc.date.available | 2018-10-03T04:44:00Z | |
dc.date.issued | 2018-10-01 | |
dc.identifier.issn | 0008-6363 | |
dc.identifier.uri | https://www.repository.cam.ac.uk/handle/1810/283043 | |
dc.description.abstract | Interleukin 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.medium | ||
dc.language | eng | |
dc.publisher | Oxford University Press (OUP) | |
dc.subject | Endothelial Cells | |
dc.subject | Immune System | |
dc.subject | Animals | |
dc.subject | Humans | |
dc.subject | Cardiovascular Diseases | |
dc.subject | Diabetes Mellitus, Type 2 | |
dc.subject | Obesity | |
dc.subject | Inflammation | |
dc.subject | Inflammation Mediators | |
dc.subject | Cell Communication | |
dc.subject | Signal Transduction | |
dc.subject | Lipid Metabolism | |
dc.subject | Biomarkers | |
dc.subject | Interleukin-33 | |
dc.subject | Interleukin-1 Receptor-Like 1 Protein | |
dc.title | Conflicting vascular and metabolic impact of the IL-33/sST2 axis. | |
dc.type | Article | |
prism.endingPage | 1594 | |
prism.issueIdentifier | 12 | |
prism.publicationDate | 2018 | |
prism.publicationName | Cardiovasc Res | |
prism.startingPage | 1578 | |
prism.volume | 114 | |
dc.identifier.doi | 10.17863/CAM.30406 | |
dcterms.dateAccepted | 2018-06-28 | |
rioxxterms.versionofrecord | 10.1093/cvr/cvy166 | |
rioxxterms.licenseref.uri | http://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.licenseref.startdate | 2018-10 | |
dc.contributor.orcid | Mallat, Ziad [0000-0003-0443-7878] | |
dc.identifier.eissn | 1755-3245 | |
rioxxterms.type | Journal Article/Review | |
pubs.funder-project-id | British Heart Foundation (RG/15/11/31593) | |
pubs.funder-project-id | British Heart Foundation (PG/15/99/31865) | |
cam.issuedOnline | 2018-07-02 | |
rioxxterms.freetoread.startdate | 2019-10-31 |
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