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10.1016/j.ejphar.2020.173620

http://scihub22266oqcxt.onion/10.1016/j.ejphar.2020.173620
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suck abstract from ncbi


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pmid33038418      Eur+J+Pharmacol 2021 ; 890 (ä): 173620
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  • Targeting pivotal inflammatory pathways in COVID-19: A mechanistic review #MMPMID33038418
  • Yarmohammadi A; Yarmohammadi M; Fakhri S; Khan H
  • Eur J Pharmacol 2021[Jan]; 890 (ä): 173620 PMID33038418show ga
  • As an emerging global health crisis, coronavirus disease 2019 (COVID-19) has been labeled a worldwide pandemic. Growing evidence is revealing further pathophysiological mechanisms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Amongst these dysregulated pathways inflammation seems to play a more critical role toward COVID-19 complications. In the present study, precise inflammatory pathways triggered by SARS-CoV-2, along with potential therapeutic candidates have been discussed. Prevailing evidence has indicated a close correlation of inflammatory cascades with severity, pathological progression, and organ damages in COVID-19 patients. From the mechanistic point of view, interleukin-6, interleukin-1beta receptor, interferon-gamma, tumor necrosis factor-alpha receptor, toll-like receptor, receptor tyrosine kinases, growth factor receptor, Janus kinase/signal transducers and transcription pathway, mammalian target of rapamycin, cytokine storm and macrophage activation have shown to play critical roles in COVID-19 complications. So, there is an urgent need to provide novel mechanistic-based anti-inflammatory agents. This review highlights inflammatory signaling pathways of SARS-CoV-2. Several therapeutic targets and treatment strategies have also been provided in an attempt to tackle COVID-19 complications.
  • |*COVID-19 Drug Treatment[MESH]
  • |*SARS-CoV-2[MESH]
  • |Anti-Inflammatory Agents/*therapeutic use[MESH]
  • |COVID-19/immunology[MESH]
  • |Humans[MESH]


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