KLF4公司
运行x2
血管平滑肌
骨桥蛋白
基因敲除
生物
细胞生物学
磷酸盐
钙化
高磷血症
分子生物学
化学
作者
Tadashi Yoshida,Mitsuaki Yamashita,Matsuhiko Hayashi
标识
DOI:10.1074/jbc.m112.361360
摘要
Background: Elucidation of molecular mechanisms controlling vascular calcification is critical for chronic kidney disease patients.Results: High phosphate induced Klf4 expression in SMCs. Klf4 knockdown attenuated high phosphate-induced SMC phenotypic switching into osteogenic cells.Conclusion: Results suggest that Klf4 contributes to high phosphate-induced conversion of SMCs into osteogenic cells.Significance: Control of Klf4 might be a novel therapeutic target for vascular calcification. Background: Elucidation of molecular mechanisms controlling vascular calcification is critical for chronic kidney disease patients. Results: High phosphate induced Klf4 expression in SMCs. Klf4 knockdown attenuated high phosphate-induced SMC phenotypic switching into osteogenic cells. Conclusion: Results suggest that Klf4 contributes to high phosphate-induced conversion of SMCs into osteogenic cells. Significance: Control of Klf4 might be a novel therapeutic target for vascular calcification.
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