慢性肾脏病血管钙化机制的研究进展。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2024-10-11 DOI:10.1002/jcp.31464
Ziyang Wang, Zebin Gui, Lirong Zhang, Zhongqun Wang
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引用次数: 0

摘要

钙磷代谢紊乱、尿毒症毒素蓄积、炎症和氧化应激以及细胞衰老等一系列因素导致血管平滑肌细胞成骨细胞样分化、细胞外囊泡分泌和钙调节因子失衡,共同促进了慢性肾脏病血管钙化的发生。表观遗传学的最新进展为研究 VC 病因学提供了更好的工具,也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 病理生理学机制的理解,还为优化临床预测指标和探索潜在治疗靶点提供了宝贵的线索。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。通过全面分析,我们期望为今后针对 CKD VC 的具体机制、临床预测指标的建立和潜在治疗策略的开发提供坚实的理论基础和研究方向。
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Advances in the mechanisms of vascular calcification in chronic kidney disease.

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.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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