ROS implicated in diabetes-associated platelet hyperactivity

Reactive oxygen species (ROS) produced endogenously or in response to an environmental stress have long been associated with a variety of tissue injuries such as ischemic heart disease and stroke. Cells exposed to that form of stress can either respond via different defense mechanisms or die by necrosis or apoptosis. At low levels, however, ROS act as signaling molecules in several intracellular processes and can, for example, increase cytosolic Ca²⁺ to the level required for activating platelets (Miyata et al., 2011). In their publication in the American Journal of Physiology and Cell Physiology, Dr. Wai Ho Tang and colleagues from Yale University School of Medicine demonstrated that human platelet aggregation and activation are sensitive to glucose concentration, and that aldose reductase contributes to this aggregation under both normal and high glucose conditions through generation of ROS (measured using Enzo’s Total ROS/Superoxide detection kit), phosphorylation of PKC isoforms and p38α MAPK, and release of thromboxane. Looking further into this pathway, urine samples from patients with platelet activation showed increased levels of 11-dehydro-TXB2, a thromboxane metabolite. Interestingly, this increase was even more substantial in diabetic patients. These results demonstrated that a complex regulatory pathway involving oxidative stress plays an important role in thromboxane-induced platelet hyperactivity and that therapies targeting aldose reductase may go a long way toward a better management of cardiovascular events.

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