端粒
细胞老化
生物
疾病
端粒酶
癌症
长寿
损耗
遗传学
医学
基因
病理
牙科
作者
Elizabeth H. Blackburn,Elissa S. Epel,Jue Lin
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2015-12-04
卷期号:350 (6265): 1193-1198
被引量:1243
标识
DOI:10.1126/science.aab3389
摘要
Telomeres are the protective end-complexes at the termini of eukaryotic chromosomes. Telomere attrition can lead to potentially maladaptive cellular changes, block cell division, and interfere with tissue replenishment. Recent advances in the understanding of human disease processes have clarified the roles of telomere biology, especially in diseases of human aging and in some aging-related processes. Greater overall telomere attrition predicts mortality and aging-related diseases in inherited telomere syndrome patients, and also in general human cohorts. However, genetically caused variations in telomere maintenance either raise or lower risks and progression of cancers, in a highly cancer type-specific fashion. Telomere maintenance is determined by genetic factors and is also cumulatively shaped by nongenetic influences throughout human life; both can interact. These and other recent findings highlight both causal and potentiating roles for telomere attrition in human diseases.
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