衰老
内源性逆转录病毒
内生
生物
逆转录病毒
细胞生物学
病毒学
下调和上调
遗传学
基因
基因表达
基因组
内分泌学
心理压抑
作者
Xiaoqian Liu,Zunpeng Liu,Liang Sun,Jie Ren,Zeming Wu,Xiaoyu Jiang,Qianzhao Ji,Qianran Wang,Yanling Fan,Yusheng Cai,Si Wang,Wei Li,Gang Cao,Moshi Song,Falong Lu,Weiqi Zhang,Jing Qu,Guanghui Liu
标识
DOI:10.1101/2021.02.22.432260
摘要
SUMMARY Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened and contribute to the aging process are largely unknown. In human senescent cells, we found that HERVK (HML-2), the most recently integrated human ERVs, are unlocked to transcribe viral genes and produce retrovirus-like particles (RVLPs). These HERVK RVLPs constitute a transmissible message to elicit senescence phenotypes in young cells, which can be blocked by neutralizing antibodies. Activation of ERVs was also observed in organs of aged primates and mice, as well as in human tissues and serum from the elderly. Their repression alleviates cellular senescence and tissue degeneration and, to some extent, organismal aging. These findings indicate that the resurrection of ERVs is a hallmark and driving force of cellular senescence and tissue aging. In brief Liu and colleagues uncover the ways in which de-repression of human endogenous retrovirus triggers cellular senescence and tissue aging; the findings provide fresh insights into therapeutic strategies for alleviating aging. Highlights Derepression of the endogenous retrovirus contributes to programmed aging Upregulation of HERVK triggers the innate immune response and cellular senescence Extracellular HERVK retrovirus-like particles induce senescence in young cells Endogenous retrovirus serves as a potential target to alleviate agings Graphical abstract
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