作者: D. van Heemst , P.M. den Reijer , R.G.J. Westendorp
DOI: 10.1016/J.EJCA.2007.07.011
关键词: Ageing 、 Apoptosis 、 Gerontology 、 Genome instability 、 Programmed cell death 、 Cancer research 、 Cell cycle checkpoint 、 Biology 、 Longevity 、 Cancer 、 Senescence 、 Oncology
摘要: Ageing is due to the accumulation of damage, which arises because evolved limitations in mechanisms for maintenance and repair. Accumulated damage may cause genomic instability, organisms with renewable tissues result cancer. To keep cancer at bay, two different tumour suppression evolved: caretakers gatekeepers. Caretakers protect genome against mutations, while gatekeepers induce cell death or cycle arrest potentially tumourigenic cells. It has been hypothesised that decreased activity a caretaker reduce life span, by increasing risk, effects increased gatekeeper on risk span be antagonistically pleiotropic. Apoptosis senescence will promote early-life survival curtailing development cancer, but eventually limit longevity. This article reviews evidence this hypothesis. We conclude several findings indeed hint an important role mediated processes ageing its related pathologies. The relative contribution apoptosis specific age-related pathologies remains established.