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dc.contributor.authorSokolova, Marina
dc.contributor.authorSjaastad, Ivar
dc.contributor.authorLouwe, Maria Cornelia
dc.contributor.authorAlfsnes, Katrine
dc.contributor.authorAronsen, Jan Magnus
dc.contributor.authorZhang, Lili
dc.contributor.authorHaugstad, Solveig Bjærum
dc.contributor.authorBendiksen, Bård Andre
dc.contributor.authorØgaard, Jonas
dc.contributor.authorBliksøen, Marte
dc.contributor.authorLien, Egil
dc.contributor.authorBerge, Rolf Kristian
dc.contributor.authorAukrust, Pål
dc.contributor.authorRanheim, Trine
dc.contributor.authorYndestad, Arne
dc.identifier.citationSokolova M, Sjaastad I, Louwe MC, Alfsnes K, Aronsen JM, Zhang L, Haugstad SB, Bendiksen BA, Øgaard J, Bliksøen M, Lien E, Berge RK, Aukrust P, Ranheim T, Yndestad A. NLRP3 inflammasome promotes myocardial remodeling during diet-induced obesity. Frontiers in Immunology. 2019;10:1621eng
dc.description.abstract<p>Background: Obesity is an increasingly prevalent metabolic disorder in the modern world and is associated with structural and functional changes in the heart. The NLRP3 inflammasome is an innate immune sensor that can be activated in response to endogenous danger signals and triggers activation of interleukin (IL)-1β and IL-18. Increasing evidence points to the involvement of the NLRP3 inflammasome in obesity-induced inflammation and insulin resistance, and we hypothesized that it also could play a role in the development of obesity induced cardiac alterations.</p> <p>Methods and Results: WT, Nlrp3−/−, and ASC−/− (Pycard−/−) male mice were exposed to high fat diet (HFD; 60 cal% fat) or control diet for 52 weeks. Cardiac structure and function were evaluated by echocardiography and magnetic resonance imaging, respectively. Whereas, NLRP3 and ASC deficiency did not affect the cardiac hypertrophic response to obesity, it was preventive against left ventricle concentric remodeling and impairment of diastolic function. Furthermore, whereas NLRP3 and ASC deficiency attenuated systemic inflammation in HFD fed mice; long-term HFD did not induce significant cardiac fibrosis or inflammation, suggesting that the beneficial effects of NLRP3 inflammasome deficiency on myocardial remodeling at least partly reflect systemic mechanisms. Nlrp3 and ASC (Pycard) deficient mice were also protected against obesity-induced systemic metabolic dysregulation, as well as lipid accumulation and impaired insulin signaling in hepatic and cardiac tissues.</p> <p>Conclusions: Our data indicate that the NLRP3 inflammasome modulates cardiac concentric remodeling in obesity through effects on systemic inflammation and metabolic disturbances, with effect on insulin signaling as a potential mediator within the myocardium.</p>eng
dc.rightsAttribution CC BYeng
dc.subjectcardiac remodelingeng
dc.subjecthigh-fat dieteng
dc.titleNLRP3 inflammasome promotes myocardial remodeling during diet-induced obesityeng
dc.typeJournal articleeng
dc.rights.holderCopyright 2019 Sokolova, Sjaastad, Louwe, Alfsnes, Aronsen, Zhang, Haugstad, Bendiksen, Øgaard, Bliksøen, Lien, Berge, Aukrust, Ranheim and Yndestad.eng
bora.peerreviewedPeer reviewedeng
dc.type.documentJournal article
dc.relation.journalFrontiers in Immunology

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