As evidence accumulates, ACE2 appears a druggable target in the attempt to limit virus entry and replication.
First-pass extracted concept
ACE2 as a druggable target for limiting SARS-CoV-2 entry and replication
Evidence Snippets
Supporting Sources
Linked Claims
Whether hypertension or ACE inhibitor and angiotensin receptor blocker use alters the fate of SARS-CoV-2 infection through effects on ACE2 density remains an open debate.
ACE2 serves as the initial cellular target of SARS-related coronaviruses including SARS-CoV-2.
SARS-CoV-2 engages ACE2 through spike protein subunit S1 for binding, while S2 induces membrane fusion and viral genome delivery.
Upon infection, ACE2 activity is reported to be reduced by downregulation or shedding, and these events might precipitate the cytokine storm of severe COVID-19.
The review describes ACE2-directed intervention strategies including receptor blockade with antibodies, small molecules, or peptides, and competitive neutralization with exogenously administered ACE2.