When cells get stressed: an integrative view of cellular senescence
When cells get stressed: an integrative view of cellular senescence
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DOI：
10.1172/jci200420663
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发表时间：
2004-01-01
影响因子：
15.9
通讯作者：
Weinberg, RA
中科院分区：
文献类型：
--
作者：
Ben-Porath, I;Weinberg, RA
进入衰老状态的细胞会经历永久性的细胞周期停滞，并伴有一系列功能和形态上的变化。细胞衰老发生在培养过程中长时间增殖之后，或者是对各种生理应激的反应，但人们对这一现象在体内所起的作用知之甚少。对衰老的研究主要集中在其作为一种限制细胞分裂的屏障这一假设的作用上，这种作用由以端粒长度形式存在的分裂计数机制所调控。在此，我们讨论细胞衰老的生物学功能，并建议应从其作为一种一般性细胞应激反应程序的角度来看待它，而不是严格地将其视为对细胞生长和分裂无限循环的一种屏障。我们还讨论了端粒缩短和端粒去帽在诱导衰老过程中所起的相对作用。
Cells entering a state of senescence undergo a permanent cell cycle arrest, accompanied by a set of functional and morphological changes. Senescence of cells occurs following an extended period of proliferation in culture or in response to various physiologic stresses, yet little is known about the role this phenomenon plays in vivo. The study of senescence has focused largely on its hypothesized role as a barrier to extended cell division, governed by a division-counting mechanism in the form of telomere length. Here, we discuss the biological functions of cellular senescence and suggest that it should be viewed in terms of its role as a general cellular stress response program, rather than strictly as a barrier to unlimited cycles of cell growth and division. We also discuss the relative roles played by telomere shortening and telomere uncapping in the induction of senescence.