细胞衰老的端粒DNA和核糖体DNA共调控假说  

Telomere DNA and ribosomal DNA co-regulation model for cell senescence

作　　者：黄必录 HUANG Bilu(Shanghai Song’s Laboratory Technology Development Co.,Ltd,Shanghai 200120,China)

机构地区：[1]上海世鹏实验室科技发展有限公司,上海200120

出　　处：《医学争鸣》2021年第3期9-15,共7页Negative

摘　　要：持续抑制抑癌蛋白P53可使细胞无限增殖,说明P53可能是调控细胞衰老的主控因子。而端粒DNA和核糖体DNA(rDNA)的拷贝数减少可能会抑制P53蛋白的降解,因此,随着染色体中端粒DNA和rDNA拷贝数的不断减少,细胞中P53蛋白的浓度就会越来越高,从而使细胞越来越衰老。端粒DNA和rDNA在转录、复制或损伤的修复过程都有可能使自身拷贝丢失,因此,沉默端粒DNA和rDNA的因子或条件能够延长细胞寿命。Continuous inhibition of tumor suppressor protein P53 can cause unlimited cell proliferation,which indicates that P53 may be a major factor in regulating cell senescence.The decrease of copy number of telomere DNA and ribosomal DNA(rDNA)can inhibit the degradation of P53 protein.Therefore,with the decrease of copy number of telomere DNA and rDNA in chromosome,the concentration of P53 protein in cells will be higher and higher,which will make cells aging.Telomere DNA and rDNA may lose their own copies in the process of transcription,replication or damage repair.Therefore,factors or conditions that silence telomere DNA and rDNA can prolong cell life.

关 键 词：衰老学说 干细胞 染色质固缩化 端粒 核糖体DNA 端粒DNA 

分 类 号：R393[医药卫生—基础医学]