Abstract
Cellular senescence induced by different stresses and telomere shortening appears to play an important role in the aging process. The products of the INK4a/ARF locus — p16INK4a and ARF — arrest cell proliferation at the senescence stage by exerting their effects on retinoblastoma protein– and p53-mediated responsive pathways. A study in this issue of the JCI provides experimental evidence of a specific upregulation of these cell cycle inhibitors in a variety of organs during mammalian aging.
Authors
Ande Satyanarayana, K. Lenhard Rudolph
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