Annual Review of Physiology· 2012Q1· Review
Aging, Cellular Senescence, and Cancer
- 2,940citations
- Q1SCImago
- 2012year
Short summary
Cellular senescence, a stress response, drives both degenerative pathologies and cancer in aging vertebrates, likely via chronic inflammation.
AI-generated from the title and abstract; the full text is not read.
Key points
- Aging promotes both degenerative pathologies (loss of function) and hyperplastic pathologies (cancer).
- Cellular senescence, a known tumor suppressor, is proposed to link these opposing aging pathologies.
- Senescence may drive aging pathologies by promoting chronic inflammation.
- The senescence response might be an example of antagonistically pleiotropic gene action.
AI-generated from the title and abstract; the full text is not read.
Abstract
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 hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
The authors' abstract, as published at the source. Annual Review of Physiology, 2012 · DOI ↗
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Field: Physiology
PhysiologyMedicine