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Am J Kidney Dis. 2013 Aug;62(2):339-51. doi: 10.1053/j.ajkd.2012.11.051. Epub 2013 Jan 26.

Chronic kidney disease: a clinical model of premature aging.

Author information

1
Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. peter.stenvinkel@ki.se

Abstract

Premature aging is a process associated with a progressive accumulation of deleterious changes over time, an impairment of physiologic functions, and an increase in the risk of disease and death. Regardless of genetic background, aging can be accelerated by the lifestyle choices and environmental conditions to which our genes are exposed. Chronic kidney disease is a common condition that promotes cellular senescence and premature aging through toxic alterations in the internal milieu. This occurs through several mechanisms, including DNA and mitochondria damage, increased reactive oxygen species generation, persistent inflammation, stem cell exhaustion, phosphate toxicity, decreased klotho expression, and telomere attrition. Because recent evidence suggests that both increased local signaling of growth factors (through the nutrient-sensing mammalian target of rapamycin) and decreased klotho expression are important modulators of aging, interventions that target these should be tested in this prematurely aged population.

KEYWORDS:

Chronic kidney disease; aging; cardiovascular disease; inflammation; klotho; mammalian target of rapamycin (mTOR); oxidative stress; phosphate

PMID:
23357108
DOI:
10.1053/j.ajkd.2012.11.051
[Indexed for MEDLINE]

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