Abstract

Cellular senescence is a state comprising an essentially irreversible proliferative arrest combined with phenotypic changes and pronounced secretory activity. Although senescence has long been linked with aging, recent studies have uncovered functional roles for senescence in embryonic development, regeneration and reprogramming, and have helped to advance our understanding of this process as a highly coordinated and programmed cellular state. In this Primer article, we summarize some of the key findings in the field and attempt to explain them in a simple model that reconciles the normal and pathological roles for senescence. We discuss how a primary role of cellular senescence is to contribute to normal development, cell plasticity and tissue repair, as a dynamic and tightly regulated cellular program. However, when this process is perturbed, the beneficial effects turn detrimental and can contribute to disease and aging.

Highlights

  • Cellular senescence is a form of permanent cell cycle arrest that can be induced in primary cells in response to a variety of stimuli

  • The controlled induction of senescence appears to be beneficial in many conditions including tumor suppression, development, reprogramming and regeneration

  • There are many avenues to explore in senescence biology

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Summary

Introduction

Cellular senescence is a form of permanent cell cycle arrest that can be induced in primary cells in response to a variety of stimuli. Staining of embryos with the senescence marker SA-ß-gal identified many tissues containing senescent cells, including the apical ectodermal ridge (AER) of the developing limb, the hindbrain roofplate, the mesonephros, the neural tube, the endolymphatic sac, the pharyngeal arches, the tip of the tail and the gut endoderm (Table 1).

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