Unité 1088 de l'Inserm, UFR de Médecine et de Pharmacie, Université de Picardie Jules Verne, Amiens, France.
Curr Opin Nephrol Hypertens. 2013 Jul;22(4):405-12. doi: 10.1097/MNH.0b013e328362155b.
This review presents new evidence related to molecular mechanisms involved in the process of cardiovascular calcification, as well as to discuss new biomarkers and novel therapeutic strategies related to vascular calcification in chronic kidney disease (CKD) patients.
microRNAs have emerged as potential players in the genesis of osteo-chondrogenic transformation, depending on the stimulus and the localization of vascular calcification. The disturbances of the fibroblast growth factor-23 (FGF23)/alpha-Klotho (Klotho) axis observed in CKD appear to play an important role in CKD-associated vascular calcification. Numerous studies have identified circulating biomarkers potentially responsible for vascular calcification and have evaluated their link with this process. The respective role of these biomarkers is not yet elucidated. Beyond phosphate binders, modulation of calcium-sensing receptor and vitamin K supplementation come into sight as new potential strategies to prevent cardiovascular calcification.
A better understanding of the molecular mechanisms which are responsible for cardiovascular calcification have led to a better detection and more adequate follow-up of this pathologic process, as well as the identification of novel therapeutic targets. Whether these new insights will lead to improved care and better survival of CKD patients with cardiovascular calcification remains to be demonstrated.
本综述介绍了心血管钙化过程中涉及的分子机制的新证据，并讨论了慢性肾脏病（CKD）患者血管钙化相关的新生物标志物和新治疗策略。
microRNAs 已成为成骨-软骨转化过程中的潜在参与者，这取决于刺激和血管钙化的定位。在 CKD 中观察到的成纤维细胞生长因子 23（FGF23）/α-Klotho（Klotho）轴的紊乱似乎在 CKD 相关的血管钙化中起重要作用。许多研究已经确定了潜在负责血管钙化的循环生物标志物，并评估了它们与该过程的联系。这些生物标志物的各自作用尚未阐明。除了磷结合剂之外，钙敏感受体的调节和维生素 K 补充也成为预防心血管钙化的新潜在策略。
对导致心血管钙化的分子机制的更好理解，导致了对这一病理过程的更好检测和更适当的随访，以及新的治疗靶点的确定。这些新的见解是否会改善 CKD 伴有心血管钙化患者的治疗效果和生存，仍有待证实。
