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).