Senescent Cells in Early Vascular Ageing and Bone Disease of Chronic Kidney Disease—A Novel Target for Treatment
1
Division of Renal Medicine, Department of Clinical Science, Technology and Intervention, Karolinska University Hospital, 14186 Stockholm, Sweden
2
Institute of Cancer Sciences, MVLS, University of Glasgow, Glasgow G61 1QH, UK
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(2), 82; https://doi.org/10.3390/toxins11020082
Received: 31 December 2018 / Revised: 23 January 2019 / Accepted: 24 January 2019 / Published: 1 February 2019
(This article belongs to the Special Issue The Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD))
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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Keywords:
chronic kidney disease; uremic toxins; senescence; Nrf2; ageing
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MDPI and ACS Style
Hobson, S.; Arefin, S.; Kublickiene, K.; Shiels, P.G.; Stenvinkel, P. Senescent Cells in Early Vascular Ageing and Bone Disease of Chronic Kidney Disease—A Novel Target for Treatment. Toxins 2019, 11, 82.
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