Key clinical risk factors include hypertension, diabetes mellitus, dyslipidemia, and hyperuricemia, while pathological drivers encompass inflammation, hyperphosphatemia, uremic toxins, and deficiency of calcification inhibitors (e.g., fetuin-A, matrix Gla protein [MGP], and pyrophosphate) that promote VSMC transdifferentiation into osteoblast-like cells (39). Here, AHSG is linked to hypertensive disorder.