Figure Legends
Figure 1. A schema identifying the tissues impacted by
SARS-CoV-2 infection and COVID-19 pathobiology . Dashed arrows identify
events whose role is as-yet unclear
Figure 2. Renin-Angiotensin signaling (RAS), Angiotensin (ANG
II) signaling, the balance between ACE1 and ACE2, and in red, the impact
of COVID-19. APs: Aminopeptidases; PREP: prolyl endopeptidase; MME:
membrane metalloendopeptidase.
Figure 3 . Hypothesized model of cell-cell communication and
pathobiology in pulmonary infection from SARS-CoV-2 and the role of
ACE1- and ACE2-derived peptides in mediating these effects on several
different cell types.
Figure 4. ACE1/ACE2 imbalance, lung injury, and factors that
determine severe pathology or mild illness. (A.) A model for the course
of COVID-19 that links ACE1/ACE2 imbalance to lung injury via the RAS
pathway and the protective role of the immune response. (B.) An
illustration of the predicted course of COVID-19 in two settings:top : Severe pathology, in patients who lack appropriate immune
response or who have prior conditions that enhance ACE1/ACE imbalance
(and RAS-induced injury). The result is increased injury that overwhelms
the adaptive immune response; bottom : Mild illness, in which
patients lack underlying conditions and can mount an appropriate immune
response, so that RAS-induced injury is less serious, an effective
immune response occurs and the infection is resolved.
Figure 5 . Hypothesized model of cell-cell communication
in myocardial infection from SARS-CoV-2 and the influence of ACE1/ACE2
imbalance on a variety of cell types involved in cardiac injury.
Figure 6. Pharmacological agents that target the RAS
pathway and counteract effects of SARS-CoV-2 infection.