PMC:7565665 / 30605-31839 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7565665","sourcedb":"PMC","sourceid":"7565665","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7565665","text":"As discussed above for other lung diseases, targeting autophagy to prevent the replication of SARS-CoV-2 is not the only potential benefit of autophagy augmentation for the treatment of COVID-19, but it may also allow the fine-tuning of optimal inflammatory responses. As now known, the pathogenesis of SARS-CoV-2-mediated severe COVID-19 involves the activation of numerous pro-inflammatory cytokines as part of the aforementioned cytokine storm causing a hyper-inflammatory state [142]. In addition to the destruction of the lungs and ARDS associated with COVID-19, this inflammatory response can cause damage to the cardiovascular, nervous, renal, hepatic, and gastrointestinal systems with wide ranging immediate and long-term consequences [142]. In support of this, studies have demonstrated the role of autophagy in the inflammatory response within the lungs and other organ systems [61]. As mentioned above, autophagy induction has been demonstrated to attenuate lung inflammation when exposed to a pathogen. Thus, autophagy induction to limit the inflammatory response, in addition to infection, has an immense therapeutic potential as an effective treatment for COVID-19 and decreasing the associated mortality and 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