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作 者:杜玉香 杨杰[2] 张玲莉 DU Yuxiang;YANG Jie;ZHANG Lingli(South China Normal University,Guangdong 510006,China;Shanghai University of Sport,Shanghai 200438,China)
机构地区:[1]华南师范大学,广州510006 [2]上海体育学院,上海200438
出 处:《中国细胞生物学学报》2021年第8期1673-1679,共7页Chinese Journal of Cell Biology
基 金:国家自然科学基金青年项目(批准号:81902298);中国博士后科学基金第14批特别资助项目(批准号:2021T140224)资助的课题。
摘 要:成纤维细胞生长因子23(fibroblast growth factor 23,FGF23)由骨骼中的成骨细胞和骨细胞分泌,作为激素样蛋白在复杂的内分泌网络中发挥核心作用,是调节细胞外基质矿化的局部骨源因子和参与矿物代谢的全身激素。FGF23主要靶向肾脏调节磷酸盐的重吸收,1,25-二羟基维生素D的产生和分解代谢以及抗衰老激素α-Klotho的表达,调节磷酸盐和维生素D动态平衡。该文具体阐述骨源性激素样FGF23对骨外器官包括肾脏、心脏、肌肉等的代谢调控,为遗传性低磷酸盐血症、高磷酸盐血症以及后天的磷酸盐代谢疾病(慢性肾脏疾病)的发病机理提供了新见解。为今后筛选基因辅助治疗提供关键性靶点,深入研究后有望为许多临床疾病提供新思路和治疗方案。FGF23(fibroblast growth factor 23)is secreted by osteoblasts and osteocytes in bone and plays a key role as hormone-like proteins in complex endocrine networks.FGF23 is not only a local bone-derived factor regulating extracellular matrix mineralization,but also a systemic hormone involved in mineral metabolism.The function of FGF23 includes the regulation of phosphate reabsorption in kidney,production and catabolism of 1,25-dihydroxyvitamin D,expression of anti-aging hormoneα-Klotho and balancing the dynamic of phosphate and vitamin D.This paper specifically describes the metabolic regulation of bone-derived hormone-like FGF23 on extraosseous organs,including kidney,heart,muscle and so on.This study provides new insights into the pathogenesis of hereditary hypophosphatemia,hyperphosphatemia and acquired phosphate metabolic diseases(chronic kidney disease).The in-depth study of FGF23 will provide a key target for screening gene-assisted therapy in the future.
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