In vivo dopamine neuron imaging-based neuroprotective small molecule screen in larval zebrafish and mechanistic investigation using conditional CRISPR knockout and cell-type-specific RNA-seq analysis, coupled with cross-species analyses including human clinical data interrogation, uncover potential disease-modifying therapeutics for Parkinson's disease (PD).

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.

Gene expression analysis reveals a novel, integrated molecular mechanism for much of the pathogenesis of COVID-19 that provides therapeutic intervention points that can be addressed with existing approved pharmaceuticals.

A novel Mendelian disease featuring early-onset hypertension is caused by a recurrent gain of function mutation in CACNA1H, which encodes the voltage-gated calcium channel Cav3.2.

Dysfunctionaladipose tissue puts obese and type 2 diabetic patients at higher risk.

Trimethylamine-oxide (TMAO), a molecule present in seafood, reduces mortality and exerts beneficial effects on the circulatory system in heart failure rats.

SWELL1 is required for basal, stretch, and flow-mediated endothelial AKT-eNOS signaling in vitro and protects against angiotensin-induced hypertension and diabetes-associated vascular dysfunction in vivo.

At least three hypothalamic subsystems are involved in cardiovascular regulation in humans.

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.