TIME, TELOMERES AND TUMORS - IS CELLULAR SENESCENCE MORE THAN AN ANTICANCER MECHANISM

被引：121

作者：

WRIGHT, WE

SHAY, JW

机构：

[1] University of Texas Southwestern Medical Center, Dept of Cell Biology and Neurosciences, Dallas, TX 75235-9039

来源：

TRENDS IN CELL BIOLOGY | 1995年 / 5卷 / 08期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/S0962-8924(00)89044-3

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Normal diploid cells, by definition, have a limited life span: they senesce after a set number of divisions both in vivo and in culture. It has been hypothesized that the molecular mechanism that measures the life span of a cell probably involves the shortening of telomeres that occurs with each round of DNA replication. This loss of telomeres is thought to induce antiproliferative signals that result in the induction of cellular senescence. In this article, Woodring Wright and Jerry Shay present a hypothesis for the mechanisms by which telomere shortening regulates cellular physiology and argue that cellular senescence is not only an anticancer mechanism but is also the cause of many of the degenerative changes of aging.

引用

页码：293 / 297

页数：5

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