cellular (relicative) senescence; senescent cell; zombie cell
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Introduction
- also see senescence-associated secretory phenotype
- In vitro:
- cessation of proliferation by multiple subcultures of cultured cells
- In vivo:
Pathology
Characterized by:
- cessation of mitosis
- telomere shortening
- tumor promoter-like activity
- enhancement of neoplastic transformation of proneoplastic cells in vivo
- expression of biomarkers for cellular senescence
- resistance to apoptosis
- senescent cells identified as excitatory neurons expressing CDKN2D contain 1.8-fold larger nuclei, more lipofuscin than CDKN2D-negative neurons & overlap with neurons containing neurofibrillary tangles in brains of patients with Alzheimer's disease[10]
- allegedly produce proinflammatory substances[6][11]
- allegedly old cells with irreversibly damaged DNA[11]
- cellular senescence contributes to sarcopenia through the accumulation of senescent cells in skeletal muscle, which secrete proinflammatory cytokines, & other bioactive molecules[13][14][15]
Notes
- senescent cells may play a role in wound healing[6]
- removal of senescent cells in young animals inhibits wound healing in young animals, but improves wound healing in old animals[6]
- cellular senescence aligns with the antagonistic pleiotropy theory of aging
- benefit for tumor suppression early in life might lead to deleterious effects later in life[9]
- see biology of aging for theories of aging
- accumulation of p16ink4a* in senescent cells may disrupt tissue structure & function & contribute to age-related pathology[2]
* p16ink4a is a marker of cells that have left the cell cycle; widely expressed, but not detected in brain or skeletal muscle
More general terms
Additional terms
References
- ↑ Eugenia Wang, University of Louisville, in: Microarray Technology and Aging Workshop, March 14, 2003
- ↑ 2.0 2.1 2.2 2.3 Baker DJ et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 2011 Nov 10; 479:232 PMID: https://pubmed.ncbi.nlm.nih.gov/22048312
Peeper DS. Old cells under attack. Nature 2011 Nov 10; 479:186 PMID: https://pubmed.ncbi.nlm.nih.gov/22071762 - ↑ Yamazaki Y, Baker DJ, Tachibana M et al Vascular Cell Senescence Contributes to Blood-Brain Barrier Breakdown. Stroke. 2016 Feb 16. PMID: https://pubmed.ncbi.nlm.nih.gov/26883501
- ↑ Campisi J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell. 2005 Feb 25;120(4):513-22. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/15734683 Free Article
- ↑ Giaimo S, d'Adda di Fagagna F. Is cellular senescence an example of antagonistic pleiotropy? Aging Cell. 2012 Jun;11(3):378-83. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/22329645 Free Article
- ↑ 6.0 6.1 6.2 6.3 Geriatric Review Syllabus, 9th edition (GRS9) Medinal-Walpole A, Pacala JT, Porter JF (eds) American Geriatrics Society, 2016
Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022 - ↑ Munoz-Espin D, Serrano M. Cellular senescence: from physiology to pathology. Nat Rev Mol Cell Biol. 2014 Jul;15(7):482-96. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/24954210
- ↑ Tchkonia T, Zhu Y, van Deursen J, Campisi J, Kirkland JL. Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. J Clin Invest. 2013 Mar;123(3):966-72. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/23454759 Free PMC Article
- ↑ 9.0 9.1 van Deursen JM. The role of senescent cells in ageing. Nature. 2014 May 22;509(7501):439-46. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/24848057 Free PMC Article
- ↑ 10.0 10.1 Dehkordi SK, Walker J, Sah E et al. Profiling senescent cells in human brains reveals neurons with CDKN2D/p19 and tau neuropathology. Nat Aging 2021 https://www.nature.com/articles/s43587-021-00142-3
- ↑ 11.0 11.1 11.2 Wajngarten M Is There Hope in the Fight Against Aging? Medscape. December 19, 2022 https://www.medscape.com/viewarticle/985809
- ↑ 12.0 12.1 12.2 Amor C, Fernandez-Maestre I, Chowdhury S et al Prophylactic and long-lasting efficacy of senolytic CAR T cells against age-related metabolic dysfunction. Nat Aging. 2024 Jan 24. PMID: https://pubmed.ncbi.nlm.nih.gov/38267706 https://www.nature.com/articles/s43587-023-00560-5
- ↑ 13.0 13.1 He Y, Xie W, Li H, Jin H, Zhang Y, Li Y. Cellular Senescence in Sarcopenia: Possible Mechanisms and Therapeutic Potential. Front Cell Dev Biol. 2022 Jan 10;9:793088. doi:http://dx.doi.org/ 10.3389/fcell.2021.793088. eCollection 2021. PMID: https://pubmed.ncbi.nlm.nih.gov/35083219 PMCID: PMC8784872 Free PMC article. Review. https://pmc.ncbi.nlm.nih.gov/articles/PMC8784872/
- ↑ 14.0 14.1 Huang Y, Wang C, Cui H, Sun G, Qi X, Yao X. Mitochondrial dysfunction in age-related sarcopenia: mechanistic insights, diagnostic advances, and therapeutic prospects. Front Cell Dev Biol. 2025 Oct 3;13:1590524. PMID: https://pubmed.ncbi.nlm.nih.gov/41113460 PMCID: PMC12531180 Free PMC article. Review. https://pmc.ncbi.nlm.nih.gov/articles/PMC12531180/
- ↑ 15.0 15.1 Forman DE, Kuchel GA, Newman JC et al Impact of Geroscience on Therapeutic Strategies for Older Adults With Cardiovascular Disease: JACC Scientific Statement. J Am Coll Cardiol. 2023 Aug 15;82(7):631-647. doi:http://dx.doi.org/ 10.1016/j.jacc.2023.05.038. Epub 2023 Jun 28. PMID: https://pubmed.ncbi.nlm.nih.gov/37389519 PMCID: PMC10414756 Free PMC article. Review. https://pmc.ncbi.nlm.nih.gov/articles/PMC10414756/