PMC:7358770 / 16116-17328 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7358770","sourcedb":"PMC","sourceid":"7358770","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7358770","text":"After the outbreak of SARS in 2003, many survivors developed residual pulmonary fibrosis with increased severity in older patients. Pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling in animal models (Fig. 5 ). Inhibition of EGFR signaling can prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections [72]. Moreover, sulfated polysaccharides such as fucoidan and sulfated rhamnan, can interfere or inhibit the expression and activation of EGFR pathway, which may help to suppress coronavirus [73,74]. The understanding of how polysaccharides play a role in EGFR and other pro-fibrotic pathways after viral infection will provide new ideas for COVID-19 treatment.\nFig. 5 The illustration about potential role of EGFR in lung fibrosis. Physical injury or a pathogen ① initiates the wound healing response by damaging healthy tissue, releasing EGFR ligands ② and activating the EGFR pathway. This results in an exaggerated wound healing response leading to a fibrotic lung ③. The early use of inhibitors like tyrosine kinase ④ could prevent the normal progress of wound healing and fibrosis 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