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).