Absence of NLRP3 Inflammasome in Hematopoietic Cells Reduces Adverse Remodeling After Experimental Myocardial Infarction
Louwe, Maria Cornelia; Olsen, Maria Belland; Kaasbøll, Ole Jørgen; Yang, Kuan; Fosshaug, Linn Elisabeth Lillerud; Alfsnes, Katrine; Øgaard, Jonas; Rashidi, Azita; Skulberg, Vidar Magne; Yang, Mingyi; Fonseca, Davi de Miranda; Sharma, Animesh; Aronsen, Jan Magnus; Schrumpf, Elisabeth; Ahmed, Muhammad Shakil; Dahl, Christen Peder; Nyman, Tuula Anneli; Ueland, Thor; Melum, Espen; Halvorsen, Bente; Bjørås, Magnar; Attramadal, Håvard; Sjaastad, Ivar; Aukrust, Pål; Yndestad, Arne
Peer reviewed, Journal article
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Original versionJACC: Basic to Translational Science. 2020, 5 (12), 1210-1224. 10.1016/j.jacbts.2020.09.013
An inflammatory response is required for tissue healing after a myocardial infarction (MI), but the process must be balanced to prevent maladaptive remodeling. This study shows that improved survival and cardiac function following MI, in mice deficient for the NLRP3 inflammasome, can be recapitulated in wild-type mice receiving bone marrow from Nlrp3−/− mice. This suggests that NLRP3 activation in hematopoietic cells infiltrating in the myocardium increases mortality and late ventricular remodeling. Our data should encourage performing clinical trials directly targeting NLRP3 inflammasome and their inflammatory cytokines (interleukin-1β and -18) in MI patients.