Apoptosis and aging: increased resistance to apoptosis enhances the aging process |
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Authors: | Email author" target="_blank">Antero?SalminenEmail author Johanna?Ojala Kai?Kaarniranta |
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Institution: | (1) Department of Neurology, Institute of Clinical Medicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland;(2) Department of Neurology, University Hospital of Kuopio, P.O. Box 1777, 70211 Kuopio, Finland;(3) Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland;(4) Department of Ophthalmology, University Hospital of Kuopio, P.O. Box 1777, 70211 Kuopio, Finland |
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Abstract: | Apoptosis is a vital component in the evolutionarily conserved host defense system. Apoptosis is the guardian of tissue integrity
by removing unfit and injured cells without evoking inflammation. However, apoptosis seems to be a double-edged sword since
during low-level chronic stress, such as in aging, increased resistance to apoptosis can lead to the survival of functionally
deficient, post-mitotic cells with damaged housekeeping functions. Senescent cells are remarkably resistant to apoptosis,
and several studies indicate that host defense mechanisms can enhance anti-apoptotic signaling, which subsequently induces
a senescent, pro-inflammatory phenotype during the aging process. At the molecular level, age-related resistance to apoptosis
involves (1) functional deficiency in p53 network, (2) increased activity in the NF-κB-IAP/JNK axis, and (3) changes in molecular
chaperones, microRNAs, and epigenetic regulation. We will discuss the molecular basis of age-related resistance to apoptosis
and emphasize that increased resistance could enhance the aging process. |
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