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Early Vascular Ageing and Cellular Senescence in Chronic Kidney Disease

Chronic kidney disease (CKD) is a clinical model of premature ageing characterized by progressive vascular disease, systemic inflammation, muscle wasting and frailty. The predominant early vascular ageing (EVA) process mediated by medial vascular calcification (VC) results in a marked discrepancy be...

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Detalles Bibliográficos
Autores principales: Dai, Lu, Qureshi, Abdul Rashid, Witasp, Anna, Lindholm, Bengt, Stenvinkel, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Research Network of Computational and Structural Biotechnology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6603301/
https://www.ncbi.nlm.nih.gov/pubmed/31303976
http://dx.doi.org/10.1016/j.csbj.2019.06.015
Descripción
Sumario:Chronic kidney disease (CKD) is a clinical model of premature ageing characterized by progressive vascular disease, systemic inflammation, muscle wasting and frailty. The predominant early vascular ageing (EVA) process mediated by medial vascular calcification (VC) results in a marked discrepancy between chronological and biological vascular age in CKD. Though the exact underlying mechanisms of VC and EVA are not fully elucidated, accumulating evidence indicates that cellular senescence - and subsequent chronic inflammation through the senescence-associated secretary phenotype (SASP) - plays a fundamental role in its initiation and progression. In this review, we discuss the pathophysiological links between senescence and the EVA process in CKD, with focus on cellular senescence and media VC, and potential anti-ageing therapeutic strategies of senolytic drugs targeting cellular senescence and EVA in CKD.