血管钙化是促进慢性肾脏病（CKD）心脑血管事件发生发展的重要因素。国内外研究和我们前期工作均证实，营养不良-炎症综合征（MICS）与醛固酮在其中扮演重要角色，而血管平滑肌细胞（VSMCs）转分化是血管钙化关键机制。我们发现醛固酮能促进血管钙化，然而，其上游调控因子不清楚。现已证实，肌肉抑制素（myostatin）、醛固酮合成酶（CYP11B2）与血管钙化密切相关。因此，我们提出以下假说：myostatin通过激活AKT/FoxO1/3通路，上调CYP11B2的水平，从而促进CKD血管钙化及VSMCs向成骨表型转分化。本研究拟采用高磷高腺嘌呤饮食建立小鼠CKD血管钙化模型，在人群、动物、细胞水平上探讨myostatin与CYP11B2对血管钙化的作用。本研究将深入剖析myostatin—CYP11B2—VSMC表型转分化—血管钙化的作用规律，为血管钙化的防治提供新策略。

Vascular calcification is an important factor of promoting the development of cardiovascular and cerebrovascular events in chronic kidney disease (CKD). Others’ and our preliminary work has confirmed that malnutrition-inflammation syndrome (MICS) plays an important role in aldosterone, and vascular smooth muscle cell (VSMC) transdifferentiation is a key mechanism of vascular calcification (VC). We found that aldosterone promotes VC. However, its upstream regulatory factor is unclear. It has been demonstrated that myostatin and the aldosterone synthase CYP11B2 are closely related to VC. Therefore, we propose the hypothesis that myostatin upregulates the levels of CYP11B2 by activating the AKT/FoxO1/3 pathway, thus promotes VC and osteogenic phenotypical change of VSMCs in CKD. This study intends to establish a CKD mice model of VC induced by a high adenine plus high phosphorus diet, and to explore the effects of myostatin and CYP11B2 on VC at population, animal, and cellular levels. The detailed mechanism for myostatin-CYP11B2-VSMC phenotypical switch-VC will be deeply investigated. The study will provide a new therapeutic intervention for VC.