Although much progress has been achieved in aging research using lower animals, especially yeast and C. elegans, aging in humans remains puzzling. Here I offer my hypothesis of host defense against age-promoting stimuli, which holds that the cell itself has a defense system and multi-organism, an even more sophisticated one against age-promoting stimuli. Here I review recent achievements in aging research and try to explain their findings in the light of my hypothesis. Age-promoting stimuli, including reactive oxygen species, telomere shortening or external stimuli such as UV or radiation induce stress responses in cells. The cellular defense system operates to overcome stimuli or repair damaged cellular components. Stress-induced damaged cells or infectious stimuli activate systemic defense systems, especially the innate immune system. Macrophages in the innate immune system are especially active not only in clearing damaged cells and repairing damaged tissue, but unfortunately, also in inducing age-related diseases.
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Curr Opin Immunol
August 2009
Department of Genetics and Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
The cancer-aging hypothesis suggests that the activation of some tumor suppressor mechanisms beneficially prevents cancer but also untowardly promotes mammalian aging. Along these lines, activation of tumor suppressor mechanisms that inhibit the cell cycle (e.g.
View Article and Find Full Text PDFNagoya J Med Sci
January 2006
Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Although much progress has been achieved in aging research using lower animals, especially yeast and C. elegans, aging in humans remains puzzling. Here I offer my hypothesis of host defense against age-promoting stimuli, which holds that the cell itself has a defense system and multi-organism, an even more sophisticated one against age-promoting stimuli.
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