CRUK London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Curr Opin Cell Biol. 2013 Dec;25(6):765-71. doi: 10.1016/j.ceb.2013.07.005. Epub 2013 Aug 1.
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, p16INK4a and p21CIP1. 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.
衰老代表着细胞周期的永久性退出，其在限制受损和潜在致癌细胞增殖方面的作用，无论是作为预防癌症的第一道防线，还是作为衰老的根本原因，都具有重要意义。视网膜母细胞瘤蛋白（RB）和 p53 肿瘤抑制因子是这一过程的核心，细胞周期蛋白依赖性激酶（CDK）抑制剂 p16INK4a 和 p21CIP1 主要实现了生长停滞。与终末分化不同，衰老通常是对多种细胞应激的普遍反应，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，其自分泌和旁分泌效应可以在组织内宣传衰老细胞的存在，并促进免疫系统清除它们。在这篇简短的综述中，我们将从细胞周期的角度强调最近在理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方面的进展。
