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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >How does proliferative homeostasis change with age? What causes it and how does it contribute to aging?
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How does proliferative homeostasis change with age? What causes it and how does it contribute to aging?

机译：增殖性体内平衡如何随年龄变化？是什么原因引起的，以及它如何导致衰老？

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The notion that there might be a cellular basis for aging stems from research that began several decades ago and was proposed to explain the loss of proliferative homeostasis, which is a hallmark of complex animals. Recent years have seen growing support for the idea that two cell fates-apoptosis and cellular senescence, both now well-established tumor suppressor mechanisms-may be important drivers of aging phenotypes and age-related disease. However, there remain many unanswered questions, some quite basic, about how these processes change with age and how they might contribute to aging. It is now clear that failures in apoptosis or senescence can result in hyperproliferative diseases such as cancer. Less is known about whether and how increased apoptosis or senescence can cause tissue degeneration and aging. In addition, there is now a growing recognition that cellular senescence can have cell-nonautonomous effects within tissues. New molecular tools and model organisms, some already on the horizon, will need to be developed to better understand the roles of apoptosis and cellular senescence in age-associated changes in proliferative homeostasis.
机译：关于衰老可能具有细胞基础的观点源于几十年前开始的研究，被提出来解释增生体内稳态的丧失，这是复杂动物的标志。近年来，越来越多的人认为两种细胞命运（细胞凋亡和细胞衰老）已成为公认的肿瘤抑制机制，这可能是衰老表型和与年龄有关的疾病的重要驱动因素。但是，关于这些过程如何随年龄变化以及它们可能如何促进衰老，仍然存在许多悬而未决的问题，其中有些是非常基本的问题。现在很清楚，凋亡或衰老的失败会导致过度增殖性疾病，例如癌症。关于增加的凋亡或衰老是否会以及如何引起组织变性和衰老，人们知之甚少。另外，现在越来越认识到细胞衰老可以在组织内具有细胞非自主效应。需要开发一些新的分子工具和模型生物，以更好地了解凋亡和细胞衰老在与年龄相关的增殖性体内平衡变化中的作用。

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