PMC:7600245 / 39638-41454 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":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome 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