ZyVersa announces publication on role of inflammasome activation

ZyVersa Therapeutics announces publication of an article in the peer-reviewed journal Circulation demonstrating the role of inflammasome NLRP3 activation in hypertrophic heart disease induced by mechanical stress. In the paper titled, “NLRP3 Inflammasome Activation Through Heart-Brain Interaction Initiates Cardiac Inflammation and Hypertrophy During Pressure Overload,” data are reported from in vivo studies in various animal models, and in vitro experiments using primary rat neonate cardiomyocytes and fibroblasts, and a human microvascular endothelial cell line. The objective was to determine the regulatory mechanism of inflammation and its role in the stressed heart. Key findings are as follows: Neural signals contribute to NLRP3 inflammasome activation in cardiac nonimmune cells that initiate inflammation in the stressed heart through IL-1beta production; Pressure overload to the heart’s left ventricle activates sympathetic efferent nerves to secrete extracellular ATP, which activates NLRP3 inflammasomes in cardiomyocytes, fibroblasts, and vascular endothelial cells, leading to L-1beta production and initiation of the inflammatory cascade that causes cardiac adaptive hypertrophy in response to mechanical stress; Cardiac afferent nerve signals also contribute to ATP secretion from SEN terminals and inflammasome activation. The above findings reveal that cardiac inflammation and hypertrophy are controlled through NLRP3 activation through heart-brain interactions.