Hydroxytyrosol attenuated obesity-induced myocardial fibrosis by inhibiting NLRP3 inflammasome-dependent pyroptosis, which downregulated CYLD and reduced NOX4-mediated oxidative stress.
Does hydroxytyrosol reduce myocardial fibrosis in obese mice?
Hydroxytyrosol attenuates obesity-induced myocardial fibrosis by modulating the NLRP3/CYLD/NOX4 oxidative stress pathway.
Hydroxytyrosol (HT), the most bioactive polyphenol in virgin olive oil, has been shown to have cardiometabolic benefits in obese rats, but the underlying mechanism has not been fully elucidated. The aim of this study was to explore the potential driving mechanism in the initiation node of obesity-induced myocardial fibrosis through in vivo and in vitro experiments, and the role of HT in obesity-induced myocardial fibrosis was investigated based on the above mechanisms. The results demonstrated that HT reduced cardiomyocyte oxidative stress and ultimately ameliorated myocardial injury and fibrosis in obese mice by inhibiting NLRP3 inflammasome-dependent pyroptosis, which in turn downregulated the deubiquitinating enzyme cylindromatosis (CYLD), thereby reducing NADPH oxidase (NOX)4 deubiquitination and promoting its degradation.
Li et al. (Sat,) conducted a other in Obesity-induced myocardial fibrosis. Hydroxytyrosol vs. High-fat diet or palmitic acid alone was evaluated on Myocardial fibrosis, oxidative stress, and pyroptosis markers. Hydroxytyrosol attenuated obesity-induced myocardial fibrosis by inhibiting NLRP3 inflammasome-dependent pyroptosis, which downregulated CYLD and reduced NOX4-mediated oxidative stress.