Does olmesartan ameliorate pressure overload-induced cardiac remodeling through inhibition of TAK1/p38 signaling in mice?
Our results suggest Olmesartan improves heart remodeling and function induced by pressure overload. P38MAPK inactivation attenuated by olmesartan via inhibition of TAK1 pathway plays an important role in the process.
These data suggest that the VDR genotype is associated with Addison's disease. The mechanisms by which distinct receptor variants might confer disease susceptibility remain to be elucidated.