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10.1016/j.mehy.2020.110415

http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.110415
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33422363!7685948!33422363
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suck abstract from ncbi


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pmid33422363      Med+Hypotheses 2021 ; 146 (ä): 110415
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  • Tackling the COVID-19 "cytokine storm" with microRNA mimics directly targeting the 3 UTR of pro-inflammatory mRNAs #MMPMID33422363
  • Gasparello J; Finotti A; Gambari R
  • Med Hypotheses 2021[Jan]; 146 (ä): 110415 PMID33422363show ga
  • COVID-19 is characterized by two major clinical phases, the SARS-CoV-2 infection of target cells and tissues, and a deep inflammatory state, known as "cytokine storm", caused by activation of pro-inflammatory genes, such as NF-kB, STAT-3, IL-6, IL-8, IL-1ss. Among possible anti-inflammatory agents, the "microRNA targeting" should be carefully considered, since it is well known that microRNAs are deeply involved in the expression of cytokines, chemokines and growth factors. The working general hypothesis is that targeting the microRNA network might be important for the development of therapeutic approaches to counteract the COVID-19 induction of inflammatory response. This hypothesis is based on several publications demonstrating the use of miRNA mimics for inhibitory effects on the production of proteins characterizing the COVID-19 "cytokine storm".
  • |*Models, Biological[MESH]
  • |3' Untranslated Regions/genetics[MESH]
  • |Anti-Inflammatory Agents/pharmacology[MESH]
  • |COVID-19/genetics/immunology/*therapy[MESH]
  • |Cytokine Release Syndrome/genetics/immunology/*therapy[MESH]
  • |Humans[MESH]
  • |Inflammation/genetics/immunology/therapy[MESH]
  • |MicroRNAs/*genetics/therapeutic use[MESH]
  • |Molecular Mimicry[MESH]
  • |RNA, Messenger/antagonists & inhibitors/genetics[MESH]


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