Papagianni Aikaterini
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Pril (Makedon Akad Nauk Umet Odd Med Nauki). 2017 Sep 1;38(2):19-27. doi: 10.1515/prilozi-2017-0018.
Fibroblast Growth Factor (FGF)-23 increase is considered one of the earliest biochemical abnormalities in chronic kidney disease-mineral bone disorder (CKD-MBD). Furthermore, accumulating data have provided evidence of a link between increased FGF-23 levels and cardiovascular morbidity and mortality in CKD patients as well as in several other populations including cardiology patients and general population. The cellular and molecular mechanisms underlying the deleterious effect of FGF-23 on the cardiovascular system are not yet completely defined and are the focus of intense research. However, animal and human studies have demonstrated important actions of FGF-23 in the heart and vessels through which could promote the development of cardiovascular complications in uremia. Moreover, significant interactions have been reported between FGF-23 and other well recognized cardiovascular risk factors such as renin-angiotensin system and inflammation which could account, at least in part, for the observed associations between FGF-23 and adverse clinical outcomes. Further studies are needed to clarify the mechanisms responsible for the pleiotropic actions of FGF-23 and moreover to identify whether it is a modifiable risk factor and a potential target of therapeutic interventions which could probably help to reduce the unacceptably high cardiovascular morbidity and mortality of CKD patients.
成纤维细胞生长因子(FGF)-23升高被认为是慢性肾脏病-矿物质和骨异常(CKD-MBD)最早出现的生化异常之一。此外,越来越多的数据表明,FGF-23水平升高与CKD患者以及包括心脏病患者和普通人群在内的其他一些人群的心血管发病率和死亡率之间存在关联。FGF-23对心血管系统产生有害作用的细胞和分子机制尚未完全明确,是深入研究的重点。然而,动物和人体研究已经证明FGF-23在心脏和血管中具有重要作用,通过这些作用可能促进尿毒症患者心血管并发症的发生。此外,据报道FGF-23与其他公认的心血管危险因素(如肾素-血管紧张素系统和炎症)之间存在显著相互作用,这至少可以部分解释FGF-23与不良临床结局之间的关联。需要进一步研究以阐明FGF-23多效性作用的机制,此外还要确定它是否是一个可改变的危险因素以及治疗干预的潜在靶点,这可能有助于降低CKD患者高得令人难以接受的心血管发病率和死亡率。