Cellular senescence: Implications for metabolic disease

被引:63
|
作者
Schafer, Marissa J. [1 ,2 ]
Miller, Jordan D. [1 ,3 ,4 ]
LeBrasseur, Nathan K. [1 ,2 ]
机构
[1] Mayo Clin, Robert & Arlene Kogod Ctr Aging, Rochester, MN 55905 USA
[2] Mayo Clin, Dept Phys Med & Rehabil, 200 First St SW, Rochester, MN 55905 USA
[3] Mayo Clin, Dept Surg, Rochester, MN 55905 USA
[4] Mayo Clin, Dept Physiol & Biomed Engn, Rochester, MN 55905 USA
关键词
Aging; Obesity; Diabetes; Exercise; Senolytics; Inflammation; GENOME-WIDE ASSOCIATION; ENDOPLASMIC-RETICULUM STRESS; INCREASED OXIDATIVE STRESS; ADIPOSE-TISSUE; SKELETAL-MUSCLE; SECRETORY PHENOTYPE; INSULIN-RESISTANCE; TELOMERE LENGTH; IN-VIVO; ENDOTHELIAL-CELLS;
D O I
10.1016/j.mce.2016.08.047
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The growing burden of obesity- and aging-related diseases has hastened the search for governing biological processes. Cellular senescence is a stress-induced state of stable growth arrest strongly associated with aging that is aberrantly activated by obesity. The transition of a cell to a senescent state is demarcated by an array of phenotypic markers, and leveraging their context-dependent presentation is essential for determining the influence of senescent cells on tissue pathogenesis. Biomarkers of senescent cells have been identified in tissues that contribute to metabolic disease, including fat, liver, skeletal muscle, pancreata, and cardiovascular tissue, suggesting that pharmacological and behavioral interventions that alter their abundance and/or behavior may be a novel therapeutic strategy. However, contradictory findings with regard to a protective versus deleterious role of senescent cells in certain contexts emphasize the need for additional studies to uncover the complex interplay that defines multi organ disease processes associated with obesity and aging. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:93 / 102
页数:10
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