BACKGROUND: The novel nonsteroidal mineralocorticoid receptor (MR) antagonist 
finerenone holds promise to be safe and efficient in the treatment of patients 
with heart failure and/or chronic kidney disease. However, its effects on 
vascular function remain elusive.
PURPOSE: The aim of this study was to determine the functional effect of 
selective MR antagonism by finerenone in vascular cells in vitro and the effect 
on vascular remodeling following acute vascular injury in vivo.
METHODS AND RESULTS: In vitro, finerenone dose-dependently reduced 
aldosterone-induced smooth muscle cell (SMC) proliferation, as quantified by 
BrdU incorporation, and prevented aldosterone-induced endothelial cell (EC) 
apoptosis, as measured with a flow cytometry based caspase 3/7 activity assay. 
In vivo, oral application of finerenone resulted in an accelerated 
re-endothelialization 3 days following electric injury of the murine carotid 
artery. Furthermore, finerenone treatment inhibited intimal and medial cell 
proliferation following wire-induced injury of the murine femoral artery 10 days 
following injury and attenuated neointimal lesion formation 21 days following 
injury.
CONCLUSION: Finerenone significantly reduces apoptosis of ECs and simultaneously 
attenuates SMC proliferation, resulting in accelerated endothelial healing and 
reduced neointima formation of the injured vessels. Thus, finerenone appears to 
provide favorable vascular effects through restoring vascular integrity and 
preventing adverse vascular remodeling.