Programmed cell death in aging

•Programmed cell death (PCD) pathways are implicated in aging and aging-related disease.•Increased PCD during mammalian aging is implicated in tissue atrophy and neurodegenerative disease.•Cancer cells and senescent cells are resistant to PCD.•Fungal life span is limited by PCD pathways. Programmed...

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Bibliographic Details
Published inAgeing research reviews Vol. 23; no. Pt A; pp. 90 - 100
Main Author Tower, John
Format Journal Article
LanguageEnglish
Published England Elsevier B.V 01.09.2015
Subjects
Aging
Aging - genetics
Aging - physiology
Animals
Apoptosis
Apoptosis - genetics
Apoptosis - physiology
Cell Death - genetics
Cell Death - physiology
Cellular Senescence
Homeostasis
Humans
Internal Medicine
Mitochondria
Necrosis
Neurodegenerative Diseases - genetics
Neurology
Sarcopenia
Senescence
Aging
Sarcopenia
Mitochondria
Senescence
Apoptosis
Necrosis
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Summary:•Programmed cell death (PCD) pathways are implicated in aging and aging-related disease.•Increased PCD during mammalian aging is implicated in tissue atrophy and neurodegenerative disease.•Cancer cells and senescent cells are resistant to PCD.•Fungal life span is limited by PCD pathways. Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.
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ISSN:1568-1637
1872-9649
1872-9649
DOI:10.1016/j.arr.2015.04.002