Abstract
Pulmonary fibrosis is a known sequela of severe or persistent lung damage. Existing clinical, imaging and autopsy studies have shown that the lungs exhibit a pathological pulmonary fibrosis phenotype after infection with coronaviruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Pulmonary fibrosis may be one of the most serious sequelae associated with coronavirus disease 2019 (COVID-19). In this study, we aimed to examine the preventative effects of the antiviral drug remdesivir on pulmonary fibrosis. We used a mouse model of bleomycin-induced pulmonary fibrosis to evaluate the effects of remdesivir on pulmonary fibrosis in vivo and further explored the potential pharmacological mechanisms of remdesivir in lung fibroblasts and alveolar epithelial cells in vitro. The preventive remdesivir treatment was started on the day of bleomycin installation, and the results showed that remdesivir significantly alleviated bleomycin-induced collagen deposition and improved pulmonary function. In vitro experiments showed that remdesivir dose-dependently suppressed TGF-β1-induced lung fibroblast activation and improved TGF-β1-induced alveolar epithelial to mesenchymal transition. Our results indicate that remdesivir can preventatively alleviate the severity of pulmonary fibrosis and provide some reference for the prevention of pulmonary fibrosis in patients with COVID-19.
Highlights
The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), was identified in December 2019 and has triggered an outbreak and spread rapidly across the world (Wang et al, 2020)
We found that the weight ratio, hydroxyproline level and percentage of fibrotic areas were significantly decreased in the remdesivir-treated group and that the inhibitory effect of remdesivir was better than that of nintedanib, while the survival rate of remdesivir was comparable to nintedanib (Figures 1B–E)
We first reported that remdesivir could attenuate BLM-induced pulmonary fibrosis by suppressing the proliferation, migration and activation of lung fibroblasts and improving alveolar epithelial to mesenchymal transition
Summary
The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), was identified in December 2019 and has triggered an outbreak and spread rapidly across the world (Wang et al, 2020). The SARS-CoV-2 pandemic brings physical and psychological burdens to patients and had a major impact on the development of all aspects of society. Most COVID-19 patients have common respiratory and gastrointestinal symptoms, such as fever, dry cough and diarrhea, and some patients may progress to severe manifestations, including acute respiratory distress syndrome (ARDS), respiratory failure, multiorgan failure, and even death (Bajwah et al, 2020; Wang et al, 2020). According to former reports, many patients survive the acute phase of ARDS but die as a result of subsequent progressive pulmonary fibrosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
