降低成纤维细胞生长因子 23 生物活性的策略。
Strategies to lower fibroblast growth factor 23 bioactivity.
机构信息
Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
出版信息
Nephrol Dial Transplant. 2022 Sep 22;37(10):1800-1807. doi: 10.1093/ndt/gfab012.
Fibroblast growth factor 23 (FGF23) is a circulating hormone derived from the bone whose release is controlled by many factors and exerts a multitude of systemic actions. There are congenital and acquired disorders of increased and decreased FGF23 levels. In chronic kidney disease (CKD), elevations of FGF23 levels can be 1000-fold above the upper physiological limit. It is still debated whether this high FGF23 in CKD is a biomarker or causally related to morbidity and mortality. Data from human association studies support pathogenicity, while experimental data are less robust. Knowledge of the biology and pathobiology of FGF23 has generated a plethora of means to reduce FGF23 bioactivity at many levels that will be useful for therapeutic translations. This article summarizes these approaches and addresses several critical questions that still need to be answered.
成纤维细胞生长因子 23（FGF23）是一种源自骨骼的循环激素，其释放受多种因素控制，并发挥多种全身作用。存在先天性和获得性的 FGF23 水平升高和降低的疾病。在慢性肾脏病（CKD）中，FGF23 水平升高可达到生理上限的 1000 倍以上。目前仍在争论 CKD 中这种高 FGF23 是生物标志物还是与发病率和死亡率有因果关系。来自人类相关性研究的数据支持其致病性，而实验数据则不太可靠。对 FGF23 的生物学和病理生物学的了解产生了许多方法，可以在多个水平上降低 FGF23 的生物活性，这对于治疗转化将非常有用。本文总结了这些方法，并讨论了仍需要回答的几个关键问题。
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