Arterial calcification (AC) is a hallmark of many serious diseases, including atherosclerosis, chronic kidney disease, and
diabetes. AC may also develop as a side-effect of therapy with anticoagulants, such as warfarin which is widely used for prophylaxis of
thrombosis. In our studies, we established the relation between warfarin-induced AC and activation of enzyme transglutaminase 2 (TG2)
and β-catenin signaling. We showed that TG2-specific inhibitor KCC-009 significantly attenuated the damaging effects of warfarin on arterial
tissue. A similar protective effect was also achieved with a dietary bioflavonoid quercetin that inhibits TG2 and β-catenin signaling.
We have shown that quercetin intercepts the chondrogenic transformation of vascular smooth muscle and also drastically attenuates calcifying
cartilaginous metaplasia in another model of AC caused by genetic loss of matrix gla protein (MGP). These findings suggest that
quercetin may be considered as a promising anti-AC therapeutic in the clinical settings of warfarin supplementation and MGP dysfunction.
Further studies are required to test the efficacy of quercetin on other types of AC.
Keywords: Arterial calcification, transglutaminase 2, β-catenin, warfarin, quercetin.
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