Wang Ziyang, Gui Zebin, Zhang Lirong, Wang Zhongqun
Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Institute of Cardiovascular Diseases, Jiangsu University, Zhenjiang, China.
J Cell Physiol. 2025 Jan;240(1):e31464. doi: 10.1002/jcp.31464. Epub 2024 Oct 11.
Vascular calcification (VC) is common in patients with advanced chronic kidney disease (CKD).A series of factors, such as calcium and phosphorus metabolism disorders, uremic toxin accumulation, inflammation and oxidative stress and cellular senescence, cause osteoblast-like differentiation of vascular smooth muscle cells, secretion of extracellular vesicles, and imbalance of calcium regulatory factors, which together promote the development of VC in CKD. Recent advances in epigenetics have provided better tools for the investigation of VC etiology and new approaches for finding more accurate biomarkers. These advances have not only deepened our understanding of the pathophysiological mechanisms of VC in CKD, but also provided valuable clues for the optimization of clinical predictors and the exploration of potential therapeutic targets. The aim of this article is to provide a comprehensive overview of the pathogenesis of CKD VC, especially the new advances made in recent years, including the various key factors mentioned above. Through the comprehensive analysis, we expect to provide a solid theoretical foundation and research direction for future studies targeting the specific mechanisms of CKD VC, the establishment of clinical predictive indicators and the development of potential therapeutic strategies.
血管钙化（VC）在晚期慢性肾脏病（CKD）患者中很常见。一系列因素，如钙磷代谢紊乱、尿毒症毒素蓄积、炎症与氧化应激以及细胞衰老，会导致血管平滑肌细胞向成骨样细胞分化、细胞外囊泡分泌以及钙调节因子失衡，这些因素共同促进了CKD中VC的发展。表观遗传学的最新进展为研究VC病因提供了更好的工具，并为寻找更准确的生物标志物提供了新方法。这些进展不仅加深了我们对CKD中VC病理生理机制的理解，还为优化临床预测指标和探索潜在治疗靶点提供了有价值的线索。本文旨在全面概述CKD VC的发病机制，尤其是近年来取得的新进展，包括上述各种关键因素。通过综合分析，我们期望为未来针对CKD VC具体机制的研究、临床预测指标的建立以及潜在治疗策略的开发提供坚实的理论基础和研究方向。
