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A growing body of evidence supports the intestinal trophism of SARS-CoV-2, with ciliated cells and intestinal enterocytes being target cells because of the high expression of ACE2 and TMPRSS2. Indeed, COVID-19 promotes a "cytokine storm" in the intestinal mucosa the resulting epithelial damage leads to increased barrier permeability, allowing the passage of gliadin in the intestinal lamina. Based on current literature, we hypothesize the role of COVID-19 as a potential trigger factor for celiac disease in predisposed patients. Genetica
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