Our results suggest that TGFBR1/TAK1 pathway-mediated vascular inflammation plays a critical role in the pathological process of vascular calcification and that FXR activation prevents the development of CKD-induced vascular inflammation and calcification via the modulation of the miR-135a-5p/TGFBR1/TAK1 pathway; this underpins the importance of FXR as a new potential target for the treatment of vascular calcification in patients with CKD. This evidence concerns the gene MAP3K7 and chronic kidney disease.