Prostaglandins are among the many inflammatory mediators that incite a cytokine storm in COVID-19 after bradykinin receptor B1 (BDKRB1) activation. This pathway mainly focuses on PGE2 and PGI2 and their interactions that lead to hyperinflammation via cytokine storms, immunothrombosis, and recruitment of fibrosis-mediating factors (VEGF, TGFB1, AREG). These pathways take place in multiple cell types, e.g. monocytes, macrophages, fibroblasts, Th17 cells, and Nk cells.