Senescent Cells in Early Vascular Ageing and Bone Disease of Chronic Kidney DiseaseA Novel Target for Treatment

被引:27
作者
Hobson, Sam [1 ]
Arefin, Samsul [1 ]
Kublickiene, Karolina [1 ]
Shiels, Paul G. [2 ]
Stenvinkel, Peter [1 ]
机构
[1] Karolinska Univ Hosp, Div Renal Med, Dept Clin Sci Technol & Intervent, S-14186 Stockholm, Sweden
[2] Univ Glasgow, Inst Canc Sci, MVLS, Glasgow G61 1QH, Lanark, Scotland
来源
TOXINS | 2019年 / 11卷 / 02期
基金
瑞典研究理事会; 欧盟地平线“2020”;
关键词
chronic kidney disease; uremic toxins; senescence; Nrf2; ageing; SMOOTH-MUSCLE-CELLS; CELLULAR SENESCENCE; INDEPENDENT PREDICTOR; PLAQUE CALCIFICATION; MEDIA CALCIFICATION; SECRETORY PHENOTYPE; INFLAMMATION; NRF2; ATHEROSCLEROSIS; CORONARY;
D O I
10.3390/toxins11020082
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Together with bone-mineral disorders, premature vascular ageing is a common feature of the uremic phenotype. A detailed understanding of mechanisms involved remains unclear and warrants further research. Available treatment options for end stage renal disease are principally dialysis and organ transplantation, as other treatment alternatives have proven insufficient. Chronic kidney disease (CKD) has been proposed as a model of early vascular and bone ageing, with accumulating evidence supporting the contribution of cellular senescence and the senescence-associated secretory phenotype (SASP) to cardiovascular pathology in CKD. Correspondingly, novel therapies based around the use of senolytic compounds and nuclear factor-erythroid-2-related factor 2 (Nrf2) agonists, have been suggested as attractive novel treatment options. In this review, we detail the contribution of the uremic environment to these processes underpinning ageing and how these relate to vascular health.
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页数:13
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