©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
Aging and uremia: Is there cellular and molecular crossover?
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
Muhammad M Yaqoob, Department of Nephrology, Barts Health NHS Trust, The Royal London Hospital, Whitechapel, E1 1BB London, United Kingdom
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
Received: June 30, 2014
Peer-review started: July 1, 2014
First decision: October 14, 2014
Revised: October 28, 2014
Accepted: November 17, 2014
Article in press: November 19, 2014
Published online: February 6, 2015
Processing time: 221 Days and 12.5 Hours
Peer-review started: July 1, 2014
First decision: October 14, 2014
Revised: October 28, 2014
Accepted: November 17, 2014
Article in press: November 19, 2014
Published online: February 6, 2015
Processing time: 221 Days and 12.5 Hours
Core Tip
Core tip: This review presents evidence that suggests that the morphological similarities between uremia and physiological aging are underpinned by similarities at a cellular and molecular level. Several of the classical cellular features of aging such as mitochondrial dysfunction and altered proteostasis have been observed in the cells and tissues of uremic humans and animals, and in in vitro models of uremia. There are also many shared features between aging and uremia in terms of cell death and survival pathways. These commonalities may present new targets for the future management of patients with chronic kidney disease.