Shay J W
University of Texas Southwestern Medical Center at Dallas, Department of Cell Biology and Neuroscience 75235-9039, USA.
Mol Med Today. 1995 Nov;1(8):378-84. doi: 10.1016/s1357-4310(95)93872-9.
There is substantial evidence for the progressive loss of the telomeric ends of chromosomes during aging, both in cell culture and in vivo. The loss of telomeres may eventually induce antiproliferative signals that result in cellular senescence. A hypothesis gaining prominence is that the activation of telomerase, a ribonucleoprotein enzyme that is important in maintaining telomere length stability, is necessary for the sustained growth of most tumors. The interrelationships between telomere shortening and aging, and how activation of telomerase may be necessary for cells to become immortal and malignant, are reviewed here.
在细胞培养和体内研究中,均有大量证据表明衰老过程中染色体端粒末端会逐渐丢失。端粒的丢失最终可能会诱导抗增殖信号,从而导致细胞衰老。一个日益受到关注的假说是,端粒酶(一种对维持端粒长度稳定性至关重要的核糖核蛋白酶)的激活是大多数肿瘤持续生长所必需的。本文综述了端粒缩短与衰老之间的相互关系,以及端粒酶激活对于细胞永生化和恶性转化的必要性。