Aging and uremia:Is there cellular and molecular crossover?
Many observers have noted that the morphological changes that occur in chronic kidney disease(CKD) patients resemble those seen in the geriatric population, with strikingly similar morbidity and mortality profiles and rates of frailty in the two groups, and shared characteristics at a pathophysiolog...
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Published in | World journal of nephrology Vol. 4; no. 1; pp. 19 - 30 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Baishideng Publishing Group Inc
06.02.2015
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Subjects | |
Online Access | Get full text |
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Summary: | Many observers have noted that the morphological changes that occur in chronic kidney disease(CKD) patients resemble those seen in the geriatric population, with strikingly similar morbidity and mortality profiles and rates of frailty in the two groups, and shared characteristics at a pathophysiological level especially in respect to the changes seen in their vascular andimmune systems. However, whilst much has been documented about the shared physical characteristics of aging and uremia, the molecular and cellular similarities between the two have received less attention. In order to bridge this perceived gap we have reviewed published research concerning the common molecular processes seen in aging subjects and CKD patients, with specific attention to altered proteostasis, mitochondrial dysfunction, post-translational protein modification, and senescence and telomere attrition. We have also sought to illustrate how the cell death and survival pathways apoptosis, necroptosis and autophagy are closely interrelated, and how an understanding of these overlapping pathways is helpful in order to appreciate the shared molecular basis behind the pathophysiology of aging and uremia. This analysis revealed many common molecular characteristics and showed similar patterns of cellular dysfunction. We conclude that the accelerated aging seen in patients with CKD is underpinned at the molecular level, and that a greater understanding of these molecular processes might eventually lead to new much needed therapeutic strategies of benefit to patients with renal disease. |
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Bibliography: | William E White;Muhammad M Yaqoob;Steven M Harwood;Queen Mary University of London,Translational Medicine and Therapeutics,William Harvey Research Institute,John Vane Science Centre,EC1M 6BQ London,United Kingdom;Department of Nephrology,Barts Health NHS Trust,The Royal London Hospital,Whitechapel,E1 1BB London,United Kingdom ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Author contributions: All authors contributed to this work. Correspondence to: Steven M Harwood, PhD, Queen Mary University of London, Translational Medicine and Therapeutics, William Harvey Research Institute, John Vane Science Centre, Charterhouse Square, EC1M 6BQ London, United Kingdom. s.m.harwood@qmul.ac.uk Telephone: +44-020-78822122 Fax: +44-020-78828252 |
ISSN: | 2220-6124 2220-6124 |
DOI: | 10.5527/wjn.v4.i1.19 |