生物技术进展 ›› 2025, Vol. 15 ›› Issue (5): 828-838.DOI: 10.19586/j.2095-2341.2025.0084

• 进展评述 • 上一篇    下一篇

慢性肾脏病患者血管钙化的机制研究

李海芳1(), 朱艳华2()   

  1. 1.湖北省阳新县人民医院肝胆外科,湖北 黄石 435200
    2.湖北省阳新县人民医院神经内科,湖北 黄石 435200
  • 收稿日期:2025-07-15 接受日期:2025-09-05 出版日期:2025-09-25 发布日期:2025-11-11
  • 通讯作者: 朱艳华
  • 作者简介:李海芳 E-mail: 270276145@qq.com

Mechanistic Insights into Vascular Calcification in Chronic Kidney Disease Patients

Haifang LI1(), Yanhua ZHU2()   

  1. 1.Department of Hepatobiliary Surgery,Yangxin County People's Hospital,Hubei Huangshi 435200,China
    2.Department of Neurology,Yangxin County People's Hospital,Hubei Huangshi 435200,China
  • Received:2025-07-15 Accepted:2025-09-05 Online:2025-09-25 Published:2025-11-11
  • Contact: Yanhua ZHU

摘要:

慢性肾脏病(chronic kidney disease, CKD)患者常发生血管钙化(vascular calcification, VC),这是导致其心血管疾病(cardiovascular disease,CVD)高发的主要原因。血管平滑肌细胞(vascular smooth muscle cells, VSMC)向成骨样细胞的转分化是VC的核心环节,受高磷血症、炎症及尿毒症毒素等复杂因素调控,但其精确分子机制尚不明确。综述了CKD背景下VC的病理机制,重点探讨了VSMC成骨样表型转化等VC的核心机制。血管钙化的发生发展受到表观遗传、细胞应激、细胞衰老等多层次的调控,这些改变相互影响,共同构成了血管钙化进展的关键驱动因素。深入阐明VSMC表型转化的分子机制,不仅可为CKD相关VC提供精准治疗靶点,还能为开发新型干预手段奠定理论基础,最终改善患者心血管疾病预后和生存质量。

关键词: 慢性肾脏病, 血管钙化, 血管平滑肌细胞, 成骨样转分化

Abstract:

Vascular calcification (VC) is a prevalent complication in patients with chronic kidney disease (CKD) and a major contributor to their high cardiovascular disease (CVD). A central event in VC is the transdifferentiation of vascular smooth muscle cells (VSMC) into an osteoblast-like phenotype. This process is driven by complex factors including hyperphosphatemia, inflammation, and uremic toxins. However, its precise molecular mechanisms remain elusive. This review summarized the pathological mechanisms of VC in the context of CKD, focusing on the osteogenic phenotypic transformation of VSMC. Furthermore, the pathogenesis of VC involves epigenetic modifications, cellular stress, and senescence. These alterations interact and collectively drive disease progression. A deeper understanding of the molecular mechanisms underlying VSMC phenotypic transformation is crucial, as it will not only identify precise therapeutic targets for CKD-related VC but also lay a theoretical foundation for developing novel interventions, with the ultimate goal of improving patients' cardiovascular outcomes and quality of life.

Key words: chronic kidney disease, vascular calcification, vascular smooth muscle cells, osteoblast-like transition

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