Physiological and pathological consequences of cellular senescence

Cellular senescence, a permanent state of cell cycle arrest accompanied by a complex phenotype, is an essential mechanism that limits tumorigenesis and tissue damage. In physiological conditions, senescent cells can be removed by the immune system, facilitating tumor suppression and wound healing. H...

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Bibliographic Details
Published in:Cellular and molecular life sciences : CMLS 2014-11, Vol.71 (22), p.4373-4386
Main Authors: Burton, Dominick G. A, Krizhanovsky, Valery
Format: Article
Language:English
Subjects:
Anatomy & physiology
Biochemistry
Biomedical and Life Sciences
Biomedicine
carcinogenesis
Cell Biology
cell cycle checkpoints
cell senescence
Cell Transformation, Neoplastic
Cellular biology
Cellular Senescence
DNA Damage
Extracellular Matrix - metabolism
Humans
Immune system
Life Sciences
Neoplasms - metabolism
Neoplasms - pathology
Pathology
phenotype
phenotypes
Progeria - metabolism
Progeria - physiopathology
Review
senescence
Signal Transduction
tissue repair
Werner Syndrome - metabolism
Werner Syndrome - physiopathology
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Summary:Cellular senescence, a permanent state of cell cycle arrest accompanied by a complex phenotype, is an essential mechanism that limits tumorigenesis and tissue damage. In physiological conditions, senescent cells can be removed by the immune system, facilitating tumor suppression and wound healing. However, as we age, senescent cells accumulate in tissues, either because an aging immune system fails to remove them, the rate of senescent cell formation is elevated, or both. If senescent cells persist in tissues, they have the potential to paradoxically promote pathological conditions. Cellular senescence is associated with an enhanced pro-survival phenotype, which most likely promotes persistence of senescent cells in vivo. This phenotype may have evolved to favor facilitation of a short-term wound healing, followed by the elimination of senescent cells by the immune system. In this review, we provide a perspective on the triggers, mechanisms and physiological as well as pathological consequences of senescent cells.
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-014-1691-3