激活素受体 IIA 配体陷阱在慢性肾脏病中的作用：一种药物预防 2 种并发症——甚至更多？

Activin receptor IIA ligand trap in chronic kidney disease: 1 drug to prevent 2 complications-or even more?

机构信息

Division of Nephrology, Ambroise Paré Hospital, APHP, Versailles Saint-Quentin-en-Yvelines University (Paris-Ile-de-France-Ouest University), Boulogne Billancourt/Paris, France; Inserm U-1018, Team 5, Paris-Sud University and Versailles Saint-Quentin-en-Yvelines University (Paris-Ile-de-France-Ouest University), Villejuif, France.

Inserm U-1018, Team 5, Paris-Sud University and Versailles Saint-Quentin-en-Yvelines University (Paris-Ile-de-France-Ouest University), Villejuif, France.

出版信息

Kidney Int. 2016 Jun;89(6):1180-2. doi: 10.1016/j.kint.2016.02.006.

DOI:10.1016/j.kint.2016.02.006

PMID:27181771

Abstract

Vascular calcification and kidney fibrosis are 2 important features of chronic kidney disease. Bone morphogenetic proteins/growth differentiation factors and their receptors are implicated in the pathogenesis of both processes. Modulation of the bone morphogenetic protein/growth differentiation factor pathways by a soluble chimeric protein that contains the activin receptor IIA (ActRIIA) domain and acts as an ActRIIA ligand trap for activin and other ligands could become a new therapeutic strategy for vascular calcification and kidney fibrosis in chronic kidney disease.

摘要

血管钙化和肾脏纤维化是慢性肾脏病的两个重要特征。骨形态发生蛋白/生长分化因子及其受体参与了这两个过程的发病机制。通过含有激活素受体 IIA（ActRIIA）结构域的可溶性嵌合蛋白来调节骨形态发生蛋白/生长分化因子途径，该蛋白作为激活素和其他配体的 ActRIIA 配体陷阱，可能成为慢性肾脏病中血管钙化和肾脏纤维化的新治疗策略。