NLRP3 and fibrosis: Furthermore, it has been found that in a mouse model of transverse aortic constriction (TAC), expression of NLRP3 inflammasome was increased in the heart, and cardiomyocyte-specific CaMKIIδ deletion decreased NLRP3 inflammasome levels in cardiomyocytes, assessed by caspase-1 activity and IL-18 activation, inhibited ventricular dilation and contractile dysfunction, and reduced cardiac fibrosis and remodeling, indicating that CaMKIIδ stimulates NLRP3 inflammasome activation in response to pressure overload (112).