Pietro Francia

TL;DR: It is reported that p66Shc−/− mice are resistant to hyperglycemia-induced, ROS-dependent endothelial dysfunction and may represent a novel therapeutic target against diabetic vascular complications.

TL;DR: The evidence so far reported and here discussed supports the concept that pharmacological modulation of p66(Shc) expression and activity may be a novel and effective target for the treatment of atherosclerotic vascular disease as well as myocardial adaptation to hypertrophic, inflammatory and neuro-hormonal stimuli in the overloaded heart.

TL;DR: It is demonstrated that, in hypertensive rats, chronic AT1R blockade is associated with an inverted vasomotor response to Ang II via AT2R-mediated NO production, which highlights the importance of the integrated Ang II receptor network, which may help to define further the mechanisms of the well-established vascular protective effects of AT 1R blockers.

TL;DR: This study aims to assess whether biventricular pacing affects plasma apelin levels in patients with severe CHF.

TL;DR: The present review focuses on the reported evidence linking p66Shc signaling pathway to high glucose-associated endothelial dysfunction, atherogenesis, nephropathy, and cardiomyopathy.