351. Senescent Cells in Early Vascular Ageing and Bone Disease of Chronic Kidney Disease—A Novel Target for Treatment
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Karolina Kublickiene, Sam Hobson, Samsul Arefin, Peter Stenvinkel, and Paul G. Shiels
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Senescence ,medicine.medical_specialty ,Aging ,senescence ,Bone disease ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,uremic toxins ,lcsh:Medicine ,Review ,030204 cardiovascular system & hematology ,Toxicology ,Bioinformatics ,Organ transplantation ,Nrf2 ,End stage renal disease ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Animals ,Humans ,Renal Insufficiency, Chronic ,Senolytic ,Vascular Calcification ,Dialysis ,Cellular Senescence ,030304 developmental biology ,0303 health sciences ,business.industry ,lcsh:R ,medicine.disease ,3. Good health ,Ageing ,ageing ,Bone Diseases ,business ,chronic kidney disease ,Kidney disease - Abstract
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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