Coronavirus disease 2019 (COVID-19), human erythrocytes and the PKC-alpha/-beta inhibitor chelerythrine -possible therapeutic implication.
Mehrdad GhashghaeiniaPeter DreischerThomas WiederMartin KöberlePublished in: Cell cycle (Georgetown, Tex.) (2020)
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19. Until now, diverse drugs have been used for the treatment of COVID-19. These drugs are associated with severe side effects, e.g. induction of erythrocyte death, named eryptosis. This massively affects the oxygen (O2) supply of the organism. Therefore, three elementary aspects should be considered simultaneously: (1) a potential drug should directly attack the virus, (2) eliminate virus-infected host cells and (3) preserve erythrocyte survival and functionality. It is known that PKC-α inhibition enhances the vitality of human erythrocytes, while it dose-dependently activates the apoptosis machinery in nucleated cells. Thus, the use of chelerythrine as a specific PKC-alpha and -beta (PKC-α/-β) inhibitor should be a promising approach to treat people infected with SARS-CoV-2.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- cell cycle arrest
- induced apoptosis
- endothelial cells
- endoplasmic reticulum stress
- cell death
- oxidative stress
- pi k akt
- induced pluripotent stem cells
- pluripotent stem cells
- signaling pathway
- drug induced
- early onset
- protein kinase
- climate change
- cord blood