Chronic Kidney Disease: A Clinical Model of Premature Aging

被引:231
作者
Stenvinkel, Peter [1 ]
Larsson, Tobias E. [1 ]
机构
[1] Karolinska Inst, Dept Clin Sci Intervent & Technol, Div Renal Med, Stockholm, Sweden
基金
英国医学研究理事会;
关键词
Chronic kidney disease; aging; cardiovascular disease; mammalian target of rapamycin (mTOR); klotho; phosphate; inflammation; oxidative stress; LEUKOCYTE TELOMERE LENGTH; PLASMA PROTEIN-A; ENDOTHELIAL PROGENITOR CELLS; MOUSE KLOTHO GENE; NAKED MOLE-RAT; CARDIOVASCULAR-DISEASE; OXIDATIVE-STRESS; RED WINE; NEGLIGIBLE SENESCENCE; HEMODIALYSIS-PATIENTS;
D O I
10.1053/j.ajkd.2012.11.051
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 2013 by the National Kidney Foundation, Inc.
引用
收藏
页码:339 / 351
页数:13
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