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The hidden role of NLRP3 inflammasome in diabesity-related COVID-19 exacerbations: lessons for drug repurposing
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  • Ilaria BertocchiOrcid,
  • Federica Foglietta,
  • Debora Collotta,
  • Carola Eva,
  • Vincenzo Brancaleone,
  • Chris Thiemermann,
  • Massimo Collino
Ilaria Bertocchi
Orcid
University of Turin
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Federica Foglietta
Universita degli Studi di Torino Scuola di Scienze della Natura
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Debora Collotta
University of Turin
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Carola Eva
University of Turin
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Vincenzo Brancaleone
University of Basilicata
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Chris Thiemermann
Queen Mary University of London Faculty of Medicine and Dentistry
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Massimo Collino
University of Turin
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Peer review status:UNDER REVIEW

25 Jun 2020Submitted to British Journal of Pharmacology
26 Jun 2020Assigned to Editor
26 Jun 2020Submission Checks Completed
29 Jun 2020Reviewer(s) Assigned

Abstract

COVID-19, the illness caused by SARS-CoV-2, has a wide-ranging clinical spectrum that, in the worst-case scenario, involves a rapid progression to severe acute respiratory syndrome and even death. Epidemiological data show that “diabesity”, the association of obesity and diabetes, is among the main risk factors associated with high morbidity and mortality. The increased susceptibility to SARS-CoV-2 infection documented in diabesity argues for initial defects in defense mechanisms, most likely due to an elevated systemic metabolic inflammation (“metaflammation”). The NLRP3 inflammasome is a master regulator of metaflammation and has a pivotal role in the pathophysiology of diabesity. Here we discuss the most recent findings suggesting contribution of NLRP3 inflammasome to the increase in complications in COVID-19 patients with diabesity. We also review current pharmacological strategies for COVID-19, focusing on treatments whose efficacy could be due, at least in part, to interference with the activation of the NLRP3 inflammasome.