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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7352545","sourcedb":"PMC","sourceid":"7352545","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7352545","text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as 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