Hasegawa Tomoka, Yamamoto Tomomaya, Hongo Hiromi, Tsuboi Kanako, Amizuka Norio
Department of Developmental Biology of Hard Tissue, Graduate School of Dental Medicine, Hokkaido University, Japan.
Clin Calcium. 2015 May;25(5):693-9.
Klotho deficient (kl/kl) mice exhibit Möncheberg's vascular calcification in the tunica media due to hyperphosphatemia and hypercalcemia by mediating the disrupted signaling of FGF23/klotho axis. Recent studies have hypothesized the mechanism of medial vascular calcification : Vascular smooth muscle cells acquired excessive intake of phosphate ions undergo a phenotypic differentiation into osteoblasts and induce biological calcification in the tunica media. It is useful to clarify the underlying cellular mechanism of vascular calcification for the development of the treatment and preventive medicine. This review will introduce the histological and ultrastructual findings on medial vascular calcification in kl/kl mice.
由于高磷血症和高钙血症通过介导FGF23/klotho轴信号紊乱，klotho基因缺陷（kl/kl）小鼠在中膜出现蒙克贝格氏血管钙化。最近的研究推测了中膜血管钙化的机制：摄入过量磷酸根离子的血管平滑肌细胞发生表型分化成为成骨细胞，并在中膜诱导生物钙化。阐明血管钙化的潜在细胞机制对于治疗和预防医学的发展很有帮助。本综述将介绍kl/kl小鼠中膜血管钙化的组织学和超微结构研究结果。
