Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6229 ER Maastricht, The Netherlands.
Laboratory of Nephrology, KU Leuven Department of Microbiology and Immunology, University Hospitals Leuven, 3000 Leuven, Belgium.
Toxins (Basel). 2020 Sep 29;12(10):624. doi: 10.3390/toxins12100624.
The cardiorenal syndrome relates to the detrimental interplay between the vascular system and the kidney. The uremic milieu induced by reduced kidney function alters the phenotype of vascular smooth muscle cells (VSMC) and promotes vascular calcification, a condition which is strongly linked to cardiovascular morbidity and mortality. Biological mechanisms involved include generation of reactive oxygen species, inflammation and accelerated senescence. A better understanding of the vasotoxic effects of uremic retention molecules may reveal novel avenues to reduce vascular calcification in CKD. The present review aims to present a state of the art on the role of uremic toxins in pathogenesis of vascular calcification. Evidence, so far, is fragmentary and limited with only a few uremic toxins being investigated, often by a single group of investigators. Experimental heterogeneity furthermore hampers comparison. There is a clear need for a concerted action harmonizing and standardizing experimental protocols and combining efforts of basic and clinical researchers to solve the complex puzzle of uremic vascular calcification.
心脏肾脏综合征涉及血管系统和肾脏之间的有害相互作用。肾功能下降引起的尿毒症环境改变了血管平滑肌细胞（VSMC）的表型，并促进血管钙化，这种情况与心血管发病率和死亡率密切相关。涉及的生物学机制包括活性氧的产生、炎症和加速衰老。对尿毒症潴留分子的血管毒性作用有更好的了解，可能会发现减少 CKD 中血管钙化的新途径。本综述旨在介绍尿毒症毒素在血管钙化发病机制中的作用的最新进展。到目前为止，证据是零碎的，而且非常有限，只有少数几种尿毒症毒素被研究，而且往往是由单个研究小组进行的。实验异质性进一步阻碍了比较。显然需要采取协调一致的行动，协调和标准化实验方案，并将基础和临床研究人员的努力结合起来，以解决尿毒症血管钙化这一复杂难题。
