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The hyperglycemic byproduct methylglyoxal impairs anticoagulant activity through covalent adduction of antithrombin III.


Jacobson RRichard , Mignemi N Nicholas , Rose K Kristie , O'Rear L Lynda , Sarilla S Suryakala , Hamm HE Heidi E , Barnett JV Joey V , Verhamme IM Ingrid M , Schoenecker J Jonathan . Thrombosis research. 2014 12 ; 134(6). 1350-7


The blood coagulation system is a tightly regulated balance of procoagulant and anticoagulant factors, disruption of which can cause clinical complications. Diabetics are known to have a hypercoagulable phenotype, along with increased circulating levels of methylglyoxal (MGO) and decreased activity of the anticoagulant plasma protein antithrombin III (ATIII). MGO has been shown to inhibit ATIII activity in vitro, however the mechanism of inhibition is incompletely understood. As such, we designed this study to investigate the kinetics and mechanism of MGO-mediated ATIII inhibition.