TY - JOUR A1 - Vaidya, Aishwarya R. A1 - Wolska, Nina A1 - Vara, Dina A1 - Mailer, Reiner Karl Walter A1 - Schröder, Katrin A1 - Pula, Giordano T1 - Diabetes and thrombosis: a central role for vascular oxidative stress T2 - Antioxidants N2 - Diabetes mellitus is the fifth most common cause of death worldwide. Due to its chronic nature, diabetes is a debilitating disease for the patient and a relevant cost for the national health system. Type 2 diabetes mellitus is the most common form of diabetes mellitus (90% of cases) and is characteristically multifactorial, with both genetic and environmental causes. Diabetes patients display a significant increase in the risk of developing cardiovascular disease compared to the rest of the population. This is associated with increased blood clotting, which results in circulatory complications and vascular damage. Platelets are circulating cells within the vascular system that contribute to hemostasis. Their increased tendency to activate and form thrombi has been observed in diabetes mellitus patients (i.e., platelet hyperactivity). The oxidative damage of platelets and the function of pro-oxidant enzymes such as the NADPH oxidases appear central to diabetes-dependent platelet hyperactivity. In addition to platelet hyperactivity, endothelial cell damage and alterations of the coagulation response also participate in the vascular damage associated with diabetes. Here, we present an updated interpretation of the molecular mechanisms underlying vascular damage in diabetes, including current therapeutic options for its control. KW - diabetes KW - oxidative stress KW - platelet hyperactivity KW - NADPH oxidase KW - NFkB KW - thrombosis KW - fibrinolysis KW - endothelial dysfunction Y1 - 2021 UR - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/62123 UR - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-621239 SN - 2076-3921 N1 - This work was funded by British Heart Foundation (PG/15/40/31522), Alzheimer’s Research UK (ARUK-PG2017A-3), and Werner Otto Foundation (#3/97) grants to Giordano Pula, and DFG grants (CRC815 TPA1 and SFB834 TPA2) to Katrin Schröder. Nina Wolska was supported by an ETIUDA7 doctoral scholarship funded by the National Science Centre, Poland (2019/32/T/NZ3/00333). VL - 10 IS - 5, art. 706 SP - 1 EP - 12 PB - MDPI CY - Basel ER -