Phenomenon characterized by the cessation of cell division
The Hayflick limit deliberates that the average cell will divide around 50 times before reaching a stage known as senescence. As the cell divides, the telomeres on the end of a linear chromosome get shorter. The telomeres will eventually no longer be present on the chromosome. This end stage is the concept that links the deterioration of telomeres to aging.Top: Primary mouse embryonic fibroblast cells (MEFs) before senescence. Spindle-shaped. Bottom: MEFs became senescent after passages. Cells grow larger, flatten shape and expressed senescence-associated β-galactosidase (SABG, blue areas), a marker of cellular senescence.
Cellular senescence is a phenomenon characterized by the cessation of cell division.[1][2][3] In their experiments during the early 1960s, Leonard Hayflick and Paul Moorhead found that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent.[4][5][6] This process is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways.[7] Cellular senescence can be initiated by a wide variety of stress inducing factors. These stress factors include both environmental and internal damaging events, abnormal cellular growth, oxidative stress, autophagy factors, among many other things.[8]
The physiological importance for cell senescence has been attributed to prevention of carcinogenesis, and more recently, aging, development, and tissue repair.[9] Senescent cells contribute to the aging phenotype, including frailty syndrome, sarcopenia, and aging-associated diseases.[10] Senescent astrocytes and microglia contribute to neurodegeneration.[11][12]
^Beausejour, C. M. (2003-08-15). "Reversal of human cellular senescence: roles of the p53 and p16 pathways". The EMBO Journal. 22 (16): 4212–4222. doi:10.1093/emboj/cdg417. ISSN 1460-2075. PMC 175806. PMID 12912919.
^Kuehnemann, Chisaka; Hughes, Jun-Wei B.; Desprez, Pierre-Yves; Melov, Simon; Wiley, Christopher D.; Campisi, Judith (2022-12-20). "Antiretroviral protease inhibitors induce features of cellular senescence that are reversible upon drug removal". Aging Cell. 22 (1): e13750. doi:10.1111/acel.13750. ISSN 1474-9718. PMC 9835573. PMID 36539941.
^Collado M, Blasco MA, Serrano M (July 2007). "Cellular senescence in cancer and aging". Cell. 130 (2): 223–233. doi:10.1016/j.cell.2007.07.003. PMID 17662938. S2CID 18689141.
^Hayat M (2014). Tumor dormancy, quiescence, and senescence, Volume 2: Aging, cancer, and noncancer pathologies. Springer. p. 188.
^Tollefsbol T (2010). Epigenetics of Aging. Springer. p. 227. ISBN 978-1-4419-0638-0.
^Shay JW, Wright WE (October 2000). "Hayflick, his limit, and cellular ageing". Nature Reviews. Molecular Cell Biology. 1 (1): 72–76. doi:10.1038/35036093. PMID 11413492. S2CID 6821048.
^van Deursen JM (May 2014). "The role of senescent cells in ageing". Nature. 509 (7501): 439–446. Bibcode:2014Natur.509..439V. doi:10.1038/nature13193. PMC 4214092. PMID 24848057.
^Cite error: The named reference pmid32752135 was invoked but never defined (see the help page).
^Rivera-Torres J, San José E (2019). "Src Tyrosine Kinase Inhibitors: New Perspectives on Their Immune, Antiviral, and Senotherapeutic Potential". Frontiers in Pharmacology. 10: 1011. doi:10.3389/fphar.2019.01011. PMC 6759511. PMID 31619990.
^Shafqat, Areez; Khan, Saifullah; Omer, Mohamed H.; Niaz, Mahnoor; Albalkhi, Ibrahem; AlKattan, Khaled; Yaqinuddin, Ahmed; Tchkonia, Tamara; Kirkland, James L.; Hashmi, Shahrukh K. (2023). "Cellular senescence in brain aging and cognitive decline". Frontiers in Aging Neuroscience. 15. doi:10.3389/fnagi.2023.1281581. ISSN 1663-4365. PMC 10702235. PMID 38076538.
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