Fig. 2
From: The role of SARS-CoV-2-mediated NF-κB activation in COVID-19 patients
The mechanism of ACE2-mediated NF-κB activation by anti-hypertension drugs and SARS-CoV-2 invasion. (middle)The inactive angiotensinogen is catalyzed to form the ANG I by the renin. Then the ANG I is converted to the ANG II by ACE, which binds to its receptor AT1R to and lead to increased blood pressure, enhanced NF-κB activation and so on. Moreover the ACE2 could catalyze the ANG I to Ang (1–9), and ANG II to Ang(1–7). Ang (1–9) could also be converted to Ang(1–7), which binds to its receptor MAS to lower blood pressure, inhibit NF-κB activation and so on. (right) Chronic treatment of ACEIs and ARBs inhibits ACE2 expression and conversion from ANG II to Ang (1–7), resulting in inhibited ANG II/AT1R and enhanced Ang(1–7)-MasR axis. (left) SARS-CoV-2 binding significantly reduces ACE2 catalytic activity through competitive inhibition, leading to increased ANG II/AT1R and inhibited Ang(1–7)-MasR axis
