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

页码：685 / 691

页数：7

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