Conclusion:
- In addition to the expression of ACE 2, the pathogenesis of COVID-19
requires the presence of further enzymes important for the replication
cycle of SARS-CoV-2
– this happens e.g. in AT 2.
- The only proven factor increasing ACE 2 expression in AT 2 is smoking
and COPD in smokers.
- However, smoking has not been proven as a risk factor for COVID-19
infection in epidemiological studies.
- There are no studies focusing on pharmacological upregulation of ACE 2
expression specifically in the pulmonary tissue. Only limited data
showing that certain drugs may increase ACE 2 expression in
extrapulmonary tissue are available, but the association with the risk
of SARS-CoV-2 infection is not known.
- It is necessary to consider the extent of the ACE 2 increase. It is
possible that some patients profit from pharmacologically-induced
upregulation of ACE 2 expression followed by cardiovascular benefits,
though the overall extent of ACE 2 expression may be lower than in the
healthy population.
- There are cautious confirmations of reduced ACE 2 expression in
comorbidities as diabetes, hypertension, and higher age. However, the
theory that decreased baseline activity of ACE 2 contributes to more
severe course of COVID-19 has not been confirmed yet.
- Increasing ACE 2 activity during COVID-19 seems to be a life-saving
strategy.