Does activation of Trpv4 reduce the hyperproliferative phenotype of cystic cholangiocytes from an animal model of ARPKD?
Taken together, our in vitro and in vivo data suggest that increasing intracellular calcium by Trpv4 activation may represent a potential therapeutic approach in PKD.
To our knowledge, these are the first results in human muscle to suggest that ACE inhibitors may augment ischemic preconditioning, possibly through B2 receptor activation.