ACE2 and viral infectious disease: The heightened “sheddase” activity of ADAM17, whether triggered by viral infection or by elevated Ang II levels and AT1R expression, leads to ectodomains of several membrane proteins being cleaved, such as TNF- α, TNFR1/2, IL-6R, VEGFR, and the ACE2 ectodomain, promoting the release of the bioactive form into the circulation [44].