In experimental models of cardiac infarction (DAMP-mediated) or endotoxemia (PAMP-mediated), activation of the NLRP3 inflammasome in either cardiac fibroblasts (36–39, 47) or myocytes (47–49) may contribute to the resultant pathology, cardiac fibroblasts being considered as the more important of the two (36–38). Here, NLRP3 is linked to serum lipopolysaccharide activity.