Stressing the cell cycle in senescence and aging
Stressing the cell cycle in senescence and aging
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DOI：
10.1016/j.ceb.2013.07.005
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发表时间：
2013-12-01
影响因子：
7.5
通讯作者：
Peters, Gordon
中科院分区：
文献类型：
--
作者：
Chandler, Hollie;Peters, Gordon
衰老代表了细胞周期的永久退出，其在减少受损和潜在致癌细胞增殖中的作用作为对抗癌症的前线防御和衰老的潜在原因都具有相关性。视网膜母细胞瘤蛋白（RB）和p53肿瘤抑制因子是该过程的核心，生长停滞主要由细胞周期蛋白依赖性激酶（CDK）抑制剂p16（INK4a）和p21（CIP1）实现。与终末分化相反，衰老是对各种细胞应激的一般反应，并且通常伴随着一组特征性的表型变化。特别值得注意的是一种分泌程序，其自分泌和旁分泌作用可以阻止组织内衰老细胞的存在，并促进免疫系统对其的清除。在这篇简短的综述中，我们将重点介绍从细胞周期的角度了解衰老和衰老之间的关系以及衰老和终末分化之间的区别的最新进展。
Senescence represents a permanent exit from the cell cycle and its role in curtailing the proliferation of damaged and potentially oncogenic cells has relevance both as a front-line defense against cancer and as an underlying cause of aging. The retinoblastoma protein (RB) and p53 tumor suppressors are central to the process and the growth arrest is primarily implemented by the cyclin-dependent kinase (CDK) inhibitors, p16(INK4a) and p21(CIP1). In contrast to terminal differentiation, senescence is a general response to a diverse range of cellular stresses and is typically accompanied by a characteristic set of phenotypic changes. Of particular note is a secretory program whose autocrine and paracrine effects can advertize the presence of senescent cells within a tissue and promote their clearance by the immune system. In this short review, we will highlight recent advances in understanding the relationship between senescence and aging and the distinction between senescence and terminal differentiation, from a cell cycle perspective.