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10.1097/MJT.0000000000001226

http://scihub22266oqcxt.onion/10.1097/MJT.0000000000001226
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32769398!ä!32769398

suck abstract from ncbi


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pmid32769398      Am+J+Ther 2020 ; 28 (3): e358-e360
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  • Shedding Light on COVID-19: ADAM17 the Missing Link? #MMPMID32769398
  • Schreiber B; Patel A; Verma A
  • Am J Ther 2020[Aug]; 28 (3): e358-e360 PMID32769398show ga
  • BACKGROUND: Coronavirus disease 2019 (COVID-19) is a rapidly expanding global health crisis. A disintegrin and metalloproteinase 17 (ADAM17), an ectodomain sheddase, is a key component of ACE2 modulation and plays a complex role in inflammation and immunosurveillance. AREAS OF UNCERTAINTY: Much remains unknown regarding the immunopathogenesis of COVID-19, including how the virus affects ADAM17 expression, activity, and regulation. SEARCH STRATEGY: Three electronic databases (MEDLINE through PubMed, Embase through Ovid, and Google Scholar) were searched to identify articles relevant to ADAM17 and severe acute respiratory syndrome coronavirus 1 and 2. Relevant articles published from January 1, 2005, to April 30, 2020, were selected, and reference lists were screened and cross-referenced. We also searched preprint studies on medRxiv and bioRxiv given the rapidly evolving data on COVID-19 SARS-CoV-2. THERAPEUTIC OPINION: Infection with SARS-CoV-2 may lead to an increase in ADAM17 sheddase activity contributing to an exuberant macrophage-predominant inflammatory response and diminished immunosurveillance capacity for viral clearance. Emerging data suggest severe lung injury in COVID-19 is associated with higher levels of TNF-alpha and IL-6, T-cell lymphopenia and exhaustion, hypercoagulability, and a macrophage-predominant immune response. This clinical picture is consistent with dysregulation of many of the molecular pathways in which ADAM17 participates. CONCLUSIONS: Elucidation of the role of ADAM17 in COVID-19 may identify novel molecular targets for drug development and therapeutic repurposement.
  • |*ADAM17 Protein/immunology/metabolism[MESH]
  • |*COVID-19/immunology/virology[MESH]
  • |Drug Discovery[MESH]
  • |Gene Expression[MESH]
  • |Humans[MESH]
  • |Immunity[MESH]
  • |SARS-CoV-2/*physiology[MESH]


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