Marzia Schiavoni

TL;DR: It is reported that inactivation of the p66shc gene protects against age-dependent, ROS-mediated endothelial dysfunction and may represent a novel target to prevent vascular aging.

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

TL;DR: The molecular mechanisms involved in the development and progression of diabetic vascular disease are analysed, looking for common up- or down-stream events, the ‘unifying mechanism’, that gives a more complete picture of diabetic disease.