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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。

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Activin receptor IIA ligand trap in chronic kidney disease: 1 drug to prevent 2 complications-or even more?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?
Kidney Int. 2016 Jun;89(6):1180-2. doi: 10.1016/j.kint.2016.02.006.
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Ligand trap for the activin type IIA receptor protects against vascular disease and renal fibrosis in mice with chronic kidney disease.激活素IIA型受体的配体陷阱可预防慢性肾病小鼠的血管疾病和肾纤维化。
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Ligand trap for the activin type IIA receptor. The long-sought drug to overcome the calcification paradox in CKD?激动素 IIA 型受体配体陷阱。能克服 CKD 钙化悖论的理想药物?
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Bone morphogenetic proteins.骨形态发生蛋白
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Activins bind and signal via bone morphogenetic protein receptor type II (BMPR2) in immortalized gonadotrope-like cells.激活素在永生化促性腺激素细胞样细胞中通过骨形态发生蛋白II型受体(BMPR2)结合并发出信号。
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引用本文的文献

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A muscle growth-promoting treatment based on the attenuation of activin/myostatin signalling results in long-term testicular abnormalities.基于抑制激活素/肌肉生长抑制素信号的肌肉生长促进治疗会导致长期的睾丸异常。
Dis Model Mech. 2021 Feb 19;14(2):dmm047555. doi: 10.1242/dmm.047555.
2
The Association between the Activin A Serum Level and Carotid Intima-Media Thickness in Chronic Kidney Disease Patients.慢性肾脏病患者血清激活素A水平与颈动脉内膜中层厚度的关联
Int J Nephrol. 2020 Nov 9;2020:8893653. doi: 10.1155/2020/8893653. eCollection 2020.
3
The systemic nature of CKD.
CKD 的系统性。
Nat Rev Nephrol. 2017 Jun;13(6):344-358. doi: 10.1038/nrneph.2017.52. Epub 2017 Apr 24.