Figure Legend
Figure 1. A diagram showing the attachment of SARS-CoV-2 to the ACE2 receptors expressed on the surface of renal cells. Invasion of the kidneys by SARS-CoV-2 leads to proteinuria, hematuria, elevation in kidney function parameters (urea, creatinine, uric acid and albumin), and occlusion of renal arteries and veins as well as collapsing glomerulopathy as a result of local cytokine storm syndrome.
Figure 2. Possible mechanism of action of H2S against SARS-CoV-2. Administration of H2S donors increases endogenous production of H2S by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), 3-mecaptopyruvate sulfurtransferase (3-MST) and D-amino acid oxidase (DAO). H2S interacts with angiotensin-converting enzyme 2 (ACE2) and blocks the binding of SARS-CoV-2 to these host cell proteins, thereby inhibiting entry of the virus into the host cell. H2S also alters SARS-CoV-2 membrane and inhibits its gene transcription including inhibiting the activation of nuclear factor-kappaB (NF-κB). In addition, H2S activates antioxidant pathway, leading to increased levels of antioxidant enzymes such as glutathione (GSH), nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and superoxide dismutase (SOD), and suppressing overproduction of reactive oxygen species (ROS). Furthermore, H2S inhibits pro-inflammatory pathway, resulting in reduced production of pro-inflammatory mediators such as interleukin-1beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and intercellular adhesion molecule-1 (ICAM-1) while activating anti-inflammatory pathway which increases production of IL-10.