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.