Cellular Senescence and the Biology of Aging, Disease, and Frailty

被引:103
|
作者
LeBrasseur, Nathan K. [1 ,2 ]
Tchkonia, Tamara [1 ]
Kirkland, James L. [1 ]
机构
[1] Mayo Clin, Robert & Arlene Kogod Ctr Aging, Rochester, MN USA
[2] Mayo Clin, Dept Phys Med & Rehabil, Rochester, MN USA
基金
美国国家卫生研究院;
关键词
THERAPEUTIC OPPORTUNITIES; OLDER-ADULTS; CELLS; INFLAMMATION; POPULATION; CANCER; AGE; IMMUNOSENESCENCE; PHENOTYPE; BIOMARKER;
D O I
10.1159/000382054
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Population aging simultaneously highlights the remarkable advances in science, medicine, and public policy, and the formidable challenges facing society. Indeed, aging is the primary risk factor for many of the most common chronic diseases and frailty, which result in profound social and economic costs. Population aging also reveals an opportunity, i.e. interventions to disrupt the fundamental biology of aging could significantly delay the onset of age-related conditions as a group, and, as a result, extend the healthy life span, or health span. There is now considerable evidence that cellular senescence is an underlying mechanism of aging and age-related conditions. Cellular senescence is a process in which cells lose the ability to divide and damage neighboring cells by the factors they secrete, collectively referred to as the senescence-associated secretory phenotype ( SASP). Herein, we discuss the concept of cellular senescence, review the evidence that implicates cellular senescence and SASP in age-related deterioration, hyperproliferation, and inflammation, and propose that this underlying mechanism of aging may play a fundamental role in the biology of frailty. (C) 2015 Nestec Ltd., Vevey/S. Karger AG, Basel
引用
收藏
页码:11 / 18
页数:8
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