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.

A CRISPR-based genomic screen identifies the ER cargo receptor SURF4 as a key determinant in the secretion of PCSK9, a protein that regulates human cholesterol levels and cardiovascular disease risk.

COPII vesicles regulate the metabolism of cholesterol through the selective transport of secretory proteins.

Mice modelling atherosclerosis show neurovascular breakdown in the cortex compared to healthy controls, and inducing atherosclerosis in mice modelling Alzheimer's disease increases the number of amyloid plaques in the hippocampus.

Dispatched cleavage, mediated by Furin, regulates Dispatched membrane trafficking and release of Sonic Hedgehog ligand.

A two-sample Mendelian randomization study suggested a potential causal relationship between HMGCR inhibition and the reduced risk of COVID-19 hospitalization.

Inactivation of SURF4 leads to impaired secretion of PCSK9 and apolipoproteins resulting in low plasma cholesterol without detrimental consequences to the liver.

Identifying why statins differ from other major lipid modifiers has revealed a new modifiable target of intervention for cardiovascular disease relevant to both drug development and optimal statin use.

Genetic evidence in humans suggests that statins reduce cancer risk via a cholesterol-independent pathway.