Cell proliferation, cell death and aging
- PMID: 2488297
- DOI: 10.1007/BF03323871
Cell proliferation, cell death and aging
Abstract
An integrated view of the processes which most likely play a critical role in the aging process at the cellular level is proposed. Cells are continuously exposed to a variety of internal and external stressors, potentially dangerous for the maintenance of the functional integrity of the cell (UV and gamma radiation, heat, oxygen free radicals, glucose, bacteria, viruses). In the course of evolution a number of mechanisms [DNA repair, production of heat shock and other stress proteins, enzymatic and non-enzymatic antioxidant defence systems, poly(ADP-ribose) polymerase activation] have emerged which allow the cell to cope with such a variety of potentially harmful agents. These mechanisms are in fact interconnected and constitute a network of cellular defence systems. It is suggested that they play a physiological role, being involved in the control of gene expression. A failure of these mechanisms does not allow the cell to maintain homeostasis and has profound consequences as far as two of the major programs of the cell are concerned, i.e. cell proliferation and cell death. Recent data suggesting that these are two physiologically active phenomena tightly linked and regulated are examined. Thus, activation of cell cycle related genes and active inhibition of suicide genes appear to be a part of an integrated process. Conversely, deprivation of growth factors seems able to induce an active process of programmed cell death characterized by Ca++,Mg+(+)-dependent endonuclease activity and DNA fragmentation (apoptosis). Similar phenomena have been shown to accompany the terminal differentiation process in several cellular systems. The understanding of the factors which favour or prevent cell death (a phenomenon which has been recognized as one of the most important in fetal development and morphogenesis) will help to unravel and eventually to manipulate the aging process. In an evolutionary perspective, cell senescence appears to be the price paid to avoid unlimited capability of proliferation, i.e. cell transformation and cancer.
Similar articles
-
Apoptosis--programmed cell death: a role in the aging process?Am J Clin Nutr. 1992 Jun;55(6 Suppl):1208S-1214S. doi: 10.1093/ajcn/55.6.1208S. Am J Clin Nutr. 1992. PMID: 1590258 Review.
-
Cell proliferation and apoptosis in the immune system in the elderly.Immunol Res. 2000;21(1):31-8. doi: 10.1385/IR:21:1:31. Immunol Res. 2000. PMID: 10803881 Review.
-
Acetylcarnitine and cellular stress response: roles in nutritional redox homeostasis and regulation of longevity genes.J Nutr Biochem. 2006 Feb;17(2):73-88. doi: 10.1016/j.jnutbio.2005.03.027. Epub 2005 Oct 18. J Nutr Biochem. 2006. PMID: 16413418 Review.
-
What does cell death have to do with aging?J Am Geriatr Soc. 1997 Sep;45(9):1140-6. doi: 10.1111/j.1532-5415.1997.tb05981.x. J Am Geriatr Soc. 1997. PMID: 9288026 Review.
-
Heat shock proteins in the photobiology of human skin.J Photochem Photobiol B. 2001 Oct;63(1-3):70-7. doi: 10.1016/s1011-1344(01)00203-2. J Photochem Photobiol B. 2001. PMID: 11684453 Review.
Cited by
-
Human POLD1 modulates cell cycle progression and DNA damage repair.BMC Biochem. 2015 Jun 19;16:14. doi: 10.1186/s12858-015-0044-7. BMC Biochem. 2015. PMID: 26087769 Free PMC article.
-
Restoration of Aqueous Humor Outflow Following Transplantation of iPSC-Derived Trabecular Meshwork Cells in a Transgenic Mouse Model of Glaucoma.Invest Ophthalmol Vis Sci. 2017 Apr 1;58(4):2054-2062. doi: 10.1167/iovs.16-20672. Invest Ophthalmol Vis Sci. 2017. PMID: 28384726 Free PMC article.
-
Two different pathways for necrotic cell death induced by free radicals.Cell Biol Toxicol. 1993 Apr-Jun;9(2):119-30. doi: 10.1007/BF00757574. Cell Biol Toxicol. 1993. PMID: 8242428
-
Vegetables and Their Bioactive Compounds as Anti-Aging Drugs.Molecules. 2022 Apr 2;27(7):2316. doi: 10.3390/molecules27072316. Molecules. 2022. PMID: 35408714 Free PMC article. Review.
-
Immunology of Aging: the Birth of Inflammaging.Clin Rev Allergy Immunol. 2023 Apr;64(2):109-122. doi: 10.1007/s12016-021-08899-6. Epub 2021 Sep 18. Clin Rev Allergy Immunol. 2023. PMID: 34536213 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Medical