Journal: Cells
Article Title: Calcium Signals during SARS-CoV-2 Infection: Assessing the Potential of Emerging Therapies
doi: 10.3390/cells11020253
Figure Lengend Snippet: Strategies for inhibition of cellular calcium transport systems involved in viral infection cascades. Calcium levels dictate the activity of the NLRP3 inflammasome, eventually leading to pyroptosis of the cell. CCBs have been shown to interact with TRP, L-type Ca 2+ channels as well as ACE2 and thus have the potential to inhibit SARS-CoV-2 endocytosis. Auxora is a specific inhibitor of the STIM/Orai system, which has been implicated in inflammation-induced injury of pulmonary endothelial cells as well as proinflammatory cytokine storms that contribute to severe COVID-19 disease. There is evidence that TRPML2 channels have a role in the endocytosis of SARS-CoV-2 into host cells. Potential drugs designed for these channels could be strong tools in the treatment of COVID-19. CBD decreases expression of ACE2 and TMPRSS2, which are both integral players in SARS-CoV-2 infection. Double-membrane vesicles (DMVs) are derived from ER membranes and formed by non-structural proteins (NSPs) 3–6 to facilitate viral RNA replication in separate compartments, as it would be impaired by immune-responses in the cytosol. HSP27 vaccination might attenuate inflammation and increase tissue regeneration. Inhibition of ERp57 might impair correct spike-folding during virus replication. Knockout/knockdown of the Sigma-1 receptor has been shown to reduce viral replication, Numbers in bubbles denote sections describing the indicated proteins and mechanisms in detail.
Article Snippet: Besides the state-of-the-art COVID-19 treatment drug Remdesivir, and potential antiviral drugs in different stages of testing such as Molnupiravir and Paxlovid, calcium channel blockers might be beneficial for treatment by modulating different pathological pathways of infected cells.
Techniques: Inhibition, Infection, Activity Assay, Expressing, Derivative Assay, Knock-Out