IDO1 deletion exacerbates arterial calcification through kynurenine insufficiency, which promotes RUNX2-mediated osteogenic reprogramming of vascular smooth muscle cells.
Kynurenine, an IDO1-mediated tryptophan metabolism main product, promotes RUNX2 ubiquitination and subsequently leads to its proteasomal degradation via an aryl hydrocarbon receptor-dependent nongenomic pathway. Insufficient kynurenine exerts the deleterious role of IDO1 ablation in promoting RUNX2-mediated VSMCs osteogenic reprogramming and calcification in vivo.
Ouyang et al. (Mon,) studied this question.