شذوذات الصفيحات لدى المرضى السكريين من النمط الثاني

Abstract EN

Type 2 diabetes mellitus (DM) is a common disease, that accounts for about 90% of diabetes, and affects more than 170 million individuals worldwide and is rapidly increasing, with projections of >350 million by 2030.

With improved control over other cardiovascular risk factors, the burden of cardiovascular disease attributable to DM is increasing.

Platelet hyperactivation and hyperaggregation play a pivotal role in the development of angiopathy in diabetic patients.

A number of mechanisms involved in platelet activation are altered in diabetes.

Platelets from type 2 diabetic patients show an enhanced endogenous reactive oxygen species production and a reduced antioxidant capability, which increase the activity of several tyrosine kinases, such as the Bruton's tyrosine kinase, MAP kinases or proteins of the SRC family.

Oxidative stress is also involved in the abnormal intracellular calcium homeostasis observed in platelets from type 2 diabetics, including an enhanced resting cytosolic calcium concentration and calcium release and entry in response to agonists.

Moreover, diabetes alters the bioavailability of nitric oxide in platelets.

Basal nitric oxide synthase activity is reduced in of platelets obtained from patients with type 2 diabetes mellitus.

The study of these abnormalities might be helpful in the development of new pharmacological strategies to reduce platelet activation in type 2 diabetes mellitus.