Aging, cellular senescence, and cancer.
Aging, cellular senescence, and cancer.
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DOI：
10.1146/annurev-physiol-030212-183653
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发表时间：
2013
影响因子：
18.2
通讯作者：
Campisi J
中科院分区：
文献类型：
--
作者：
Campisi J
对于大多数物种来说，衰老促进了一系列退化病理，其特征是组织或细胞功能的衰弱丧失。然而，特别是在脊椎动物中，衰老也会促进增生性病理，其中最致命的是癌症。与以退化细胞和组织为特征的功能丧失相反，恶性(癌症)细胞必须获得新的(尽管是异常的)功能，使它们能够发展成致命的肿瘤。这篇综述讨论了这样一种观点，即尽管似乎具有相反的特征，但衰老的退行性和增生性病理至少部分与一个常见的生物学现象有关：一种被称为细胞衰老的细胞应激反应。衰老反应被广泛认为是一种有效的肿瘤抑制机制。然而，最近的证据强化了这样的观点，即它也会导致退行性和增生性病理，很可能是通过促进慢性炎症。因此，这种衰老反应可能是拮抗多效性基因作用的结果。
For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyper-plastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
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影响因子：
64.8
作者：
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通讯作者：
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