Fig. 2
From: Revisiting potential value of antitumor drugs in the treatment of COVID-19
Schematic depiction of hyperinflammatory condition and cytokine storm induced by SARS-CoV-2 infection and potential antitumor drugs to control excessive inflammation. SARS-CoV-2 infection activates macrophages, neutrophils and T lymphocytes. Macrophages and neutrophils produce and release a vast set of pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β). These cytokines lead to the activation of JAK-STAT signaling pathway in normal cells and ultimately contribute to the expression of inflammatory genes, further exaggerating the inflammatory responses. Several antitumor drugs target those cytokines and their downstream signaling pathways are considered as potential antiviral agents to control cytokine storm and excessive inflammation. Besides, the upregulation of vascular endothelial growth factor (VEGF) in patients with COVID-19 exacerbates tissue hypoxia. Bevacizumab, one of the anti-angiogenic drugs, blocks the interaction of VEGF-A and its receptor, thus suppressing angiogenesis and increasing tissue perfusion. (Created with the assistance of smart.servier.com)