Figure captions
Figure 1. Mechanism of SARS-CoV-2 entry into the host cell and QC and
HCQ action points. CQ and HCQ can interfere with the binding of the
virus to ACE-2 receptors and prevent the endosomes from maturing to the
late form. A similar process is involved in the immunomodulatory
activity of CQ and HCQ, by preventing autophagy and autoantigen
presentation by antigen-presenting cells via the endosomal pathway.
Figure 2. The Renin-Agiotensin System: Renin is activated in the
juxtaglomerular cells of the kidneys in response to decreased blood
pressure, beta-activation, or activation by macula densa cells in
response to a decreased sodium load in the distal convoluted tubule.
Once released into the blood, renin act on angiotensinogen that is
produced in the liver and continuously circulates in the plasma. Renin
cleaves angiotensinogen into angiotensin I (Ang I). ACE, which is found
primarily in the vascular endothelium of the lungs and kidneys, converts
Ang I to Ang II. After conversion, Ang II has effects on the kidneys,
adrenal cortex, arterioles, and the brain by binding to Ang II type I
(AT1) and type II (AT2) receptors. ACE-2 maintains local homeostasis by
countering the effects of Ang II.
Figure 3. Role of the renin-angiotensin-aldosterone system in
inflammatory processes triggered by the action of angiotensin II (Ang
II) on AT receptors. Infection of the cell by SARS-CoV-2 aggravates
inflammation by destroying ACE-2 receptors that counteract the effects
of Ang II and by triggering pyroptosis in the infected cell.
Figure 4. Chloroquine and hydroxychloroquine enantiomers and their
respective active metabolites: chloroquine (CQ), hydroxychloroquine
(HCQ), desethyl chloroquine (DCQ), bis-desethyl chloroquine (BDCQ), mono
desethyl hydroxychloroquine (DHCQ).