ABSTRACT This study investigated the effects of lanthanum chloride on vascular calcification associated with chronic kidney disease (CKD) and the mechanisms involved in changes in nano‐hydroxyapatite. Vascular calcification was induced in CKD rats using a high‐phosphorus diet and adenine. Human vascular smooth muscle cells (hVSMCs) were calcified in vitro using sodium β‐glycerophosphate (β‐GP) and saturated nano‐hydroxyapatite. The effects of lanthanum chloride were evaluated using various analytical methods, including serum biochemistry, EVG, Vonkossa staining, Alizarin Red staining, Ca 2+ detection, Western blotting, and transmission electron microscopy. The results showed that lanthanum chloride effectively inhibited calcium deposition and osteogenic differentiation, a finding confirmed in both in vivo and in vitro experiments. Scanning electron microscopy (SEM) analysis of the calcified crystals revealed altered crystal morphology and a decreased calcium‐to‐phosphorus ratio after treatment. X‐ray diffraction confirmed that these crystals were hydroxyapatite. Proteomic analysis indicated that the effects of lanthanum chloride were associated with apoptosis and the PPARγ/Wnt/β‐catenin signaling pathway. Lanthanum chloride inhibits apoptosis in human vascular smooth muscle cells (hVSMCs), while PPARγ inhibitors can reverse this effect. In summary, lanthanum chloride may significantly reduce vascular calcification in patients with CKD by altering the morphology of hydroxyapatite and activating PPARγ to inhibit apoptosis.
Zhang et al. (2026) studied this question.