Klotho-FGF23、心血管疾病与血管钙化：非黑即白？

Klotho-FGF23, Cardiovascular Disease, and Vascular Calcification: Black or White?

机构信息

Department of Experimental Diagnostic and Specialty Medicine (DIMES), Nephrology Dialysis and Renal Transplant Unit, S. Orsola Hospital, University of Bologna, Bologna, Italy.

Department of Health Sciences, Renal Unit, San Paolo Hospital Milan, University of Milan, Milan, Italy.

出版信息

Curr Vasc Pharmacol. 2018 Jan 26;16(2):143-156. doi: 10.2174/1570161115666170310092202.

DOI:10.2174/1570161115666170310092202

PMID:28294047

Abstract

BACKGROUND

Patients affected by Chronic Kidney Disease and Mineral Bone Disorder (CKD-MBD) have a high risk of cardiovascular (CV) mortality that is poorly explained by traditional risk factors. The newest medical treatments for CKD-MBD have been associated with encouraging, but still inconsistent, improvement in CV disease complications and patient survival. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy (LVH), atherosclerosis, and vascular calcification (VC) may help with diagnosis and treatment of the organ damage that occurs secondary to CKD-MBD, thus improving survival. Recent insights about fibroblast growth factor-23 (FGF23) and its co-receptor, Klotho, have led to marked advancement in interpreting data on vascular aging and CKDMBD.

CONCLUSION

This review will discuss the current experimental and clinical evidence regarding FGF23 and Klotho, with a particular focus on their roles in LVH, atherosclerosis, and VC.

摘要

背景

患有慢性肾脏病-矿物质和骨异常（CKD-MBD）的患者心血管（CV）死亡率较高，这不能用传统的危险因素很好地解释。CKD-MBD 的最新医学治疗方法与心血管疾病并发症和患者生存的令人鼓舞但仍不一致的改善有关。更好地了解左心室肥厚（LVH）、动脉粥样硬化和血管钙化（VC）的生物标志物和机制可能有助于诊断和治疗 CKD-MBD 引起的器官损伤，从而提高生存率。最近关于成纤维细胞生长因子 23（FGF23）及其共同受体 Klotho 的研究结果，对解释血管老化和 CKD-MBD 的相关数据有了显著的推进。