ANG II and COVID-19.
Hitherto accumulated evidences suggest that upon infected with SARS-CoV-2, the ACE2 is downregulated and as a result the ANG II level goes up in a feed-back mechanism to form Ang (1-7) and Ang (1-9) is disrupted (Vaduganathan et al., 2020). Previous studies have shown that elevated ANG II level promotes inflammation and is associated with lung injury and positively regulating the cytokine production by the activation of AT1R (Kuba et al., 2006; Wang et al., 2012). Angiotensin II can induce oxidative stress through production of reactive oxygen species (ROS) via the nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase causing oxidative stress (Guzik et al., 2007). It has been shown that a number of COVID-19 patients in the high risk group suffer from severe lung injury associated with increase in plasma ANG II level (Liu et al., 2020a).