MYD88 and hypertensive disorder: To confirm this in our study, we measured NF-κB levels and showed that Ang II increases NF-κB activity in WT mice, and this effect was attenuated in cTLR4KO mice, allowing us to believe that Ang II-induced hypertension occurs through the MyD88 dependent and independent TLR4/NF-κB signaling pathways in cardiomyocytes.