Does postconditioning protect against reperfusion injury in hypertensive dilated cardiomyopathy by activating MEK/ERK1/2 signaling?
PostC confers cardioprotection through alternative survival pathways in normal and CH hearts, and cardiac function recovery in DCM relies mainly on MEK/ERK1/2 cascade. Down-regulation of phosphatidylinositide 3-kinase does not affect the cardioprotective response in DCM, because MEK/ERK1/2 cascade may convey direct Akt activation, strengthening downstream signaling.
these results imply a role for nuclear NF-κB expression in the tumorigenesis of UUT-UC. Nuclear NF-κB may serve as a useful independent molecular marker to predict outcome and may represent a promising therapeutic target for patients with UUT-UC.