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10.1016/j.cmet.2020.09.007

http://scihub22266oqcxt.onion/10.1016/j.cmet.2020.09.007
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32941797!7486067!32941797
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suck abstract from ncbi


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pmid32941797      Cell+Metab 2020 ; 32 (5): 704-709
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  • Shining Light on the COVID-19 Pandemic: A Vitamin D Receptor Checkpoint in Defense of Unregulated Wound Healing #MMPMID32941797
  • Evans RM; Lippman SM
  • Cell Metab 2020[Nov]; 32 (5): 704-709 PMID32941797show ga
  • SARS-CoV-2 pneumonitis can quickly strike to incapacitate the lung, leading to severe disease and sometimes death. In this perspective, we suggest that vitamin D deficiency and the failure to activate the vitamin D receptor (VDR) can aggravate this respiratory syndrome by igniting a wounding response in stellate cells of the lung. The FDA-approved injectable vitamin D analog, paricalcitol, suppresses stellate cell-derived murine hepatic and pancreatic pro-inflammatory and pro-fibrotic changes. Therefore, we suggest a possible parallel program in the pulmonary stellate cells of COVID-19 patients and propose repurposing paricalcitol infusion therapy to restrain the COVID-19 cytokine storm. This proposed therapy could prove important to people of color who have higher COVID-19 mortality rates and lower vitamin D levels.
  • |*Betacoronavirus[MESH]
  • |Animals[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*drug therapy/immunology/virology[MESH]
  • |Cytokines/metabolism[MESH]
  • |Drug Repositioning/*methods[MESH]
  • |Ergocalciferols/*pharmacology/*therapeutic use[MESH]
  • |Humans[MESH]
  • |Mice[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*drug therapy/immunology/virology[MESH]
  • |Receptors, Calcitriol/*agonists/metabolism[MESH]
  • |SARS-CoV-2[MESH]
  • |Vitamin D Deficiency/drug therapy/epidemiology[MESH]


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