Abstract
The ongoing coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is posing a great threat to the global economy and public health security. Together with the acknowledged angiotensin-converting enzyme 2, glucose-regulated protein 78, transferrin receptor, AXL, kidney injury molecule-1, and neuropilin 1 are also identified as potential receptors to mediate SARS-CoV-2 infection. Therefore, how to inhibit or delay the binding of SARS-CoV-2 with the abovementioned receptors is a key step for the prevention and treatment of COVID-19. As the third gasotransmitter, hydrogen sulfide (H2S) plays an important role in many physiological and pathophysiological processes. Recently, survivors were reported to have significantly higher H2S levels in COVID-19 patients, and mortality was significantly greater among patients with decreased H2S levels. Considering that the beneficial role of H2S against COVID-19 and COVID-19-induced comorbidities and multiorgan damage has been well-examined and reported in some excellent reviews, this review will discuss the recent findings on the potential receptors of SARS-CoV-2 and how H2S modulates the above receptors, in turn blocking SARS-CoV-2 entry into host cells.
Highlights
The ongoing coronavirus disease 2019 (COVID-19) pandemic has spread worldwide to more than 200 countries/regions and has caused over 180 million infections, and over 4 million deaths globally, which continues to rise rapidly
[89] Recent evidence in the literature indicated that intra- and intermolecular disulfides in both angiotensin-converting enzyme 2 (ACE2) and SARS-CoV-2 S protein had an important role for the binding process, which was regulated by the thiol-disulfide balance of the extracellular environment. [43, 44] Using molecular dynamics simulations revealed that the reduction of all disulfides into the sulfydryl groups completely impaired the binding of the SARS-CoV-2 S protein to ACE2
Our study found that the endoplasmic reticulum (ER) stress markers, including glucose-regulated protein 78 (GRP78), CHOP, and active caspase-12 levels, were significantly elevated in the calcified rat aorta and H2S alleviated vascular calcification by inhibiting ERS through the Akt signaling pathway activation [50]
Summary
The ongoing coronavirus disease 2019 (COVID-19) pandemic has spread worldwide to more than 200 countries/regions and has caused over 180 million infections, and over 4 million deaths globally (as of 10 July 2021), which continues to rise rapidly. Together with the acknowledged angiotensin-converting enzyme 2 (ACE2), [3] glucose-regulated protein 78 (GRP78), [4] transferrin receptor (TFR), [5] AXL, [6] kidney injury molecule-1 (KIM-1) [7], and neuropilin 1 (NRP1) [8] are identified as additional potential receptors to mediate SARS-CoV-2 infection. The first step of SARS-CoV-2 infection in humans is the binding of RBD in the S1 subunit to the host’s cell surface receptors, which plays a decisive role in the invasion and spread of viruses, and, in turn, affects the clinical symptoms of patients. This review will discuss the recent findings on the potential receptors of SARS-CoV-2 and how H2S modulates the abovementioned receptors, in turn blocking SARS-CoV-2 entry into host cells
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