The kinin-kallikrein system is a crucial target for the treatment of COVID-19.

SARS-CoV-2 has evolved to cleverly mimic the FURIN-cleavage site in human ENaC-α, unlike any prior coronavirus strain, shedding new light on the Acute Respiratory Distress Syndrome (ARDS) in COVID-19 patients.

Current evidence does not suggest adverse effects of ACE inhibitors or ARBs in COVID-19 patients and, to the contrary, discontinuing these drugs in these patients may potentially be harmful.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

Patients exposed to ⍺1-AR antagonists have reduced risks of mechanical ventilation and death in lower respiratory tract infection-related illnesses, highlighting the need for prospective trials assessing ⍺1-AR antagonists' effectiveness in COVID-19.

A single neonatal inflammatory event induces long-term impairments in two forms of adult respiratory motor plasticity, an important aspect of the control of breathing for compensation after injury or disease.

Cellular and chemogenetic approaches identify a novel mode of chemotransduction involving regulation of basal breathing by CO₂/H+-dependent disinhibition.

Evidence is mounting that rare loss-of-function variants in the TLR7 gene predispose men with no medical history to severe forms of COVID-19.

The primary respiratory defect seen in aged cardiomyocytes is an elevated proton leak mediated by ANT1, and this is prevented by treatment with SS-31 (elamipretide).

Depletion of LRRC8A provides genetic evidence for the importance of Cl^- channels in NLRP3 activation.