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.
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.
The activin receptor ALK7 regulates the adaptation of brown adipose tissue to nutrient availability by preventing over-activation of signaling pathways induced by fasting, allowing appropriate response to cold exposure.
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).
