Fossel M
Department of Medicine, Michigan State University College of Human Medicine, East Lansing, USA.
JAMA. 1998 Jun 3;279(21):1732-5. doi: 10.1001/jama.279.21.1732.
Recent research has shown that inserting a gene for the protein component of telomerase into senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then display all the other identifiable characteristics of young, healthy cells. This advance not only suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechanism can be reset, extending the replicative life span of such cells and resulting in markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of malignant transformation. It is now possible to explore the fundamental cellular mechanisms underlying human aging, clarifying the role played by replicative senescence. By implication, we may soon be able to determine the extent to which the major causes of death and disability in aging populations in developed countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia--are attributable to such fundamental mechanisms. If they are amenable to prevention or treatment by alteration of cellular senescence, the clinical implications have few historic precedents.
最近的研究表明，将端粒酶蛋白质成分的基因插入衰老的人类细胞中，可使其端粒重新延长至年轻细胞的典型长度，然后这些细胞呈现出年轻、健康细胞的所有其他可识别特征。这一进展不仅表明端粒是细胞衰老的核心计时机制，还证明了这种机制可以重置，延长此类细胞的复制寿命，并产生“更年轻”（即早期传代）细胞典型的基因表达标志物，而没有恶性转化的特征。现在有可能探索人类衰老背后的基本细胞机制，阐明复制性衰老所起的作用。这意味着，我们或许很快就能确定发达国家老年人群主要死亡和残疾原因——癌症、动脉粥样硬化、骨关节炎、黄斑变性和阿尔茨海默病痴呆症——在多大程度上可归因于这些基本机制。如果它们可以通过改变细胞衰老来预防或治疗，那么其临床意义几乎没有历史先例。
