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Aging as a catabolic malfunction
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Geriatric .
Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
2004 (English)In: International Journal of Biochemistry and Cell Biology, ISSN 1357-2725, E-ISSN 1878-5875, Vol. 36, no 12, 2365-2375 p.Article, review/survey (Refereed) Published
Abstract [en]

Cellular degradative processes, which include lysosomal (autophagic) and proteasomal degradation, as well as catabolism of proteins by cytosolic and mitochondrial proteases, provide for a continuous turnover of cellular components, such as damaged or obsolete biomolecules and organelles. Inherent insufficiency of these degradative processes results in progressive accumulation within long-lived postmitotic cells of biological 'garbage' (waste material), such as various oxidized proteins, functionally effete mitochondria, and lipofuscin (age pigment), an intralysosomal, polymeric, undegradable material. There is increasing evidence that lipofuscin hampers lysosomal degradative capacity, thus promoting the aggravation of accumulated damage at old age. Being rich in redox-active iron, lipofuscin granules also may exacerbate oxidative stress levels in senescent cells. Thus, increasing the efficiency of cellular degradative pathways and preventing involvement of iron in oxidant-induced lysosomal and cellular damage may be potential strategies for anti-aging interventions. © 2004 Elsevier Ltd. All rights reserved.

Place, publisher, year, edition, pages
2004. Vol. 36, no 12, 2365-2375 p.
Keyword [en]
Aging, Autophagy, Lipofuscin, Lysosomes, Oxidative stress
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-45571DOI: 10.1016/j.biocel.2004.03.009OAI: oai:DiVA.org:liu-45571DiVA: diva2:266467
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-13

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Terman, AlexeiBrunk, Ulf

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