What is the physiological function of the CoV-2 targeted ACE2-Mas receptor pathway on lung/nasal epithelial cells?

CoV-2 targets ACE2 receptor on epithelial cells, pneumocytes, as well as nasal cells which seem to be cells of the nervous system (loss of smell is a symptom of Covid).
ACE2-Receptor is rather well known for its role in blood pressure regulation.
Much less seems to be known about the role of ACE2 as a receptor of cells of pneumocytes of the lung, alternatively of nasal nerve cells (expressing neuropilin as "marker"; very new reports).

Considering that CoV-2’s destruction of ACE2-cells leads to a loss of angiotensin 1-7 and its action on Mas-receptor, what is the function of MAS-receptor signaling not primarily in blood pressure regulation but within the context of epithelia of lung, airways and nerve cell’s of the nose? What physiological function gets lost if CoV-2 destroys ACE2-cells of the lung and nose epithelia?

Refering to blood pressure:
AC Simões e Silva et al
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682698/
"Most available evidence supports a counter-regulatory role for Ang-(1-7) by opposing many actions of Ang II on AT1 receptors, especially vasoconstriction and proliferation. Many studies have now shown that Ang-(1-7) by acting via Mas receptor exerts inhibitory effects on inflammation and on vascular and cellular growth mechanisms."

Refering to asthma as related to Covid because of dry cough as a sypmtom
El-Hashim at al.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402818/
"Angiotensin-(1–7) [Ang-(1–7)] has anti-inflammatory effects in models of cardiovascular disease and arthritis, but its effects in asthma are unknown."