PMC:7600245 / 61314-62893 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7600245","sourcedb":"PMC","sourceid":"7600245","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7600245","text":"There are reports about unusually high serum ferritin in COVID-19 patients [203]. A retrospective, multicenter cohort study reported increased levels of serum ferritin in COVID-19 non-survivors compared with COVID-19 survivors [99]. The increase in serum ferritin indicates dysregulated iron homeostasis pertaining to oxidative stress and inflammatory response. Dysregulated iron homeostasis may propagate the viral infections leading to severe respiratory illnesses such as pulmonary fibrosis and acute respiratory distress syndrome [204,205,206,207]. Accordingly, the use of iron chelators, particularly deferoxamine, in managing/treating COVID-19 has been proposed [208]. Deferoxamine may exert an antiviral effect by depleting iron availability, which has been shown to play a critical role in the replication of RNA viruses such as HCV, HIV, and West Nile virus [209,210,211,212,213]. In addition to its effect on iron level, deferoxamine also appears to have immunomodulatory effects [209]. Along these lines, deferoxamine mitigated the symptoms of Enterovirus-infected mice and decreased the mortality rate. It also upregulated the B cell levels and improved the neutralizing antibody titer [209]. Deferoxamine has also been reported to in vitro block endothelial inflammation induced by influenza A infection by inhibiting IL-6 synthesis [214]. Deferoxamine may also have antifibrotic effects. An intranasal treatment with deferoxamine was reported to prevent pulmonary fibrosis and pulmonary functional decline in bleomycin-induced pulmonary fibrosis animal model 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