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Klotho, stem cells, and aging

Authors Bian A, Neyra J, Zhan M, Hu MC

Received 19 March 2015

Accepted for publication 22 May 2015

Published 4 August 2015 Volume 2015:10 Pages 1233—1243

DOI https://doi.org/10.2147/CIA.S84978

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Richard Walker

Ao Bian,1,2 Javier A Neyra,3 Ming Zhan,4 Ming Chang Hu1,3

1Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, USA; 2Department of Nephrology, First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China; 3Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, 4Methodist Hospital Research Institute, Weill Cornell Medical College, Houston, TX, USA

Abstract: Aging is an inevitable and progressive biological process involving dysfunction and eventually destruction of every tissue and organ. This process is driven by a tightly regulated and complex interplay between genetic and acquired factors. Klotho is an antiaging gene encoding a single-pass transmembrane protein, klotho, which serves as an aging suppressor through a wide variety of mechanisms, such as antioxidation, antisenescence, antiautophagy, and modulation of many signaling pathways, including insulin-like growth factor and Wnt. Klotho deficiency activates Wnt expression and activity contributing to senescence and depletion of stem cells, which consequently triggers tissue atrophy and fibrosis. In contrast, the klotho protein was shown to suppress Wnt-signaling transduction, and inhibit cell senescence and preserve stem cells. A better understanding of the potential effects of klotho on stem cells could offer novel insights into the cellular and molecular mechanisms of klotho deficiency-related aging and disease. The klotho protein may be a promising therapeutic agent for aging and aging-related disorders.

Keywords: aging, cell senescence, klotho, stem cells, Wnt
 
 

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