Angiotensin-Converting Enzyme 2 (ACE2) in the Pathogenesis of ARDS in COVID-19.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic pathways and theoretical therapeutics without new empirical data.
PubMed 35003058 · doi:10.3389/fimmu.2021.732690
What was done
This narrative review synthesized literature on the dual role of angiotensin-converting enzyme 2 (ACE2) as the host entry receptor for SARS-CoV-2 and as a protective carboxypeptidase in acute respiratory distress syndrome (ARDS), examining the rationale for recombinant ACE2 therapeutics.
What was found
The abstract reports no empirical numbers or quantitative findings. It describes mechanistic relationships: SARS-CoV-2 binds ACE2 with higher affinity than SARS-CoV, and viral infection downregulates cell-surface ACE2. Because ACE2 normally degrades angiotensin II, B1-bradykinin, and apelin to mitigate lung injury in ARDS, this downregulation is implicated in COVID-19 respiratory pathology. Soluble recombinant ACE2 serves conceptually as both a variant-agnostic decoy receptor and an enzymatic supplement.
Why it matters
It outlines why ACE2 loss of function during viral entry contributes directly to lung injury, establishing the mechanistic basis for recombinant ACE2 decoys in treating COVID-19-associated ARDS.
Limits
As a narrative review, it includes no original clinical data, systematic search protocol, or meta-analytic pooling. Abstract provides no quantitative outcomes, dosing data, or human trial efficacy results for recombinant ACE2 therapies.
Cited by
- contradicts ACE2 is normally a water channel in cells, especially in the lungs.