2020
DOI: 10.1016/j.it.2020.08.001
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Modeling Potential Autophagy Pathways in COVID-19 and Sarcoidosis

Abstract: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and mainly affects the lungs. Sarcoidosis is an autoinflammatory disease characterized by the diffusion of granulomas in the lungs and other organs. Here, we discuss how the two diseases might involve some common mechanistic cellular pathways around the regulation of autophagy.

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Cited by 23 publications
(27 citation statements)
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“…Coronaviruses have adapted by producing many strategies to escape or to benefit via the inhibition and/or stimulation of autophagy [52 ]. SARS‐Cov‐2 most likely impacts autophagy by several mechanisms [52–55 ] including highjacking the autophagy machinery for their intracellular survival (canonical) [54 ] and expressing specific proteins to usurp components of the autophagy pathway and propagate in host cells (noncanonical) [52 ].…”
Section: Introductionmentioning
confidence: 99%
“…Coronaviruses have adapted by producing many strategies to escape or to benefit via the inhibition and/or stimulation of autophagy [52 ]. SARS‐Cov‐2 most likely impacts autophagy by several mechanisms [52–55 ] including highjacking the autophagy machinery for their intracellular survival (canonical) [54 ] and expressing specific proteins to usurp components of the autophagy pathway and propagate in host cells (noncanonical) [52 ].…”
Section: Introductionmentioning
confidence: 99%
“…The mechanism of the immune response occurring in patients with active sarcoidosis and infection from SARS-CoV-2 is largely unknown, but it has been hypothesized that it could involve common cellular pathways such as those that have a crucial role in regulating the mechanism of authophagy. Host-pathogen interactions at different points of the viral life cycle seem to be important for explaining in part the heterogeneity of clinical pictures that characterize COVID-19 [ 30 ]. In sarcoidosis, the presence of a sustained stimulation of the host immune system from the antigen exposition (infectious and non-infectious) has been reported as one of the main mechanisms of formation and maintenance of sarcoid granulomas [ 31 , 32 ].…”
Section: Hypothesis Of Common Pathways Of Pathogenesis and Mechanimentioning
confidence: 99%
“…Some authors have hypothesized that some constitutional defects of the regulation of macroautophagy in patients with sarcoidosis could predispose to more severe clinical pictures if they are infected from the novel SARS-CoV-2. Some viruses such as herpes and coronaviruses could indeed benefit from the dysregulation observed in sarcoidosis and bypass some autophagy steps [ 30 ]. Furthermore, the high affinity for the angiotensin-converting enzyme (ACE)2 protein, whose polymorphisms have been associated with different disease progression and severity in sarcoidosis, and the characteristic presence of typical lymphocytes reduction in both disorders, might be some of the mechanisms that could predispose to a high severity of the disease [ 30 , 33 , 34 ].…”
Section: Hypothesis Of Common Pathways Of Pathogenesis and Mechanimentioning
confidence: 99%
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