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Comment
. 2016 Feb;65(2):349-51.
doi: 10.2337/dbi15-0032.

Platelet Dysfunction in Type 1 Diabetes: Stressing the Thromboxanes

Jaclyn A Wisinski  1 , Michelle E Kimple  2
Affiliations
Comment

Platelet Dysfunction in Type 1 Diabetes: Stressing the Thromboxanes

Jaclyn A Wisinski et al. Diabetes. 2016 Feb.
No abstract available

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Figures

Figure 1
Figure 1
Summary of the platelet activation pathways addressed in Zaccardi et al. (15) and how these may be impacted by factors in the T1DM state and aspirin prophylaxis. The arachidonic acid metabolites PGI2 and TXA2 have opposing impacts on platelet activation, with PGI2 acting through a pair of Gs-coupled G-protein–coupled receptors (GPCRs), IP1 and IP2, to inhibit downstream platelet activation. PGI2 is produced from endothelial cells in the vascular wall from the unstable intermediate, PGH2, by the enzyme prostaglandin I synthase (PTGIS). TXA2, on the other hand, is produced from PGH2 by thromboxane A synthase (TBXAS) in the platelets themselves and works through a pair of Gi- and Gq-coupled GPCRs, TPα and TPβ, to promote downstream platelet activation. PGH2 is produced by both COX-1 and COX-2, with COX-1 being of primary importance in the platelet. Zaccardi et al. (15) showed that platelet TXM is persistently elevated in adult T1DM subjects and that this correlates with increased oxidative stress but not inflammation or hyperglycemia and that production of TXA2 metabolites can be effectively ameliorated by treatment with low-dose aspirin, an irreversible and semi-selective inhibitor of COX-1. Proteins and enzymes are shown in boldface italic type and steps that are specifically revealed to be important in this T1DM population by the current study are identified by green asterisks. Further mechanistic studies will be important to confirm the specific molecular signaling pathways at play in this population.
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