Progeria, rapamycin and normal aging: recent breakthrough

被引:41
作者
Blagosklonny, Mikhail V. [1 ]
机构
[1] Roswell Pk Canc Inst, Dept Cell Stress Biol, BLSC, Buffalo, NY 14263 USA
来源
AGING-US | 2011年 / 3卷 / 07期
关键词
rapamycin; aging; progeria; senescence; autophagy; obesity; HUTCHINSON-GILFORD-PROGERIA; EXTENDS LIFE-SPAN; ONCOGENE-INDUCED SENESCENCE; HUMAN-DIPLOID FIBROBLASTS; HEMATOPOIETIC STEM-CELLS; DNA-DAMAGE RESPONSES; PROTEIN S6 KINASE; CELLULAR SENESCENCE; LAMIN-A; TELOMERE LENGTH;
D O I
10.18632/aging.100352
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
A recent discovery that rapamycin suppresses a pro-senescent phenotype in progeric cells not only suggests a non-toxic therapy for progeria but also implies its similarity with normal aging. For one, rapamycin is also known to suppress aging of regular human cells. Here I discuss four potential scenarios, comparing progeria with both normal and accelerated aging. This reveals further indications of rapamycin both for accelerated aging in obese and for progeria.
引用
收藏
页码:685 / 691
页数:7
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