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Myocyte aging and mitochondrial turnover
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: Experimental Gerontology, ISSN 0531-5565, Vol. 39, no 5, 701-705 p.Article, review/survey (Refereed) Published
Abstract [en]

Cardiac myocytes, skeletal muscle fibers, and other long-lived postmitotic cells show dramatic age-related alterations that mainly affect mitochondria and the lysosomal compartment. Mitochondria are primary sites of reactive oxygen species formation that causes progressive damage to mitochondrial DNA and proteins in parallel to intralysosomal lipofuscin accumulation. There is amassing evidence that several various mechanisms may contribute to age-related accumulation of damaged mitochondria following initial oxidative injury. Such mechanisms may include clonal expansion of defective mitochondria, decreased propensity of altered mitochondria to become autophagocytosed (due to mitochondrial enlargement or decreased membrane damage associated with weakened respiration), suppressed autophagy because of heavy lipofuscin loading of lysosomes, and decreased efficiency of Lon protease. © 2004 Elsevier Inc. All rights reserved.

Place, publisher, year, edition, pages
2004. Vol. 39, no 5, 701-705 p.
Keyword [en]
Aging, Autophagy, Lysosomes, Mitochondria, Myocardium, Oxidative stress, Postmitotic cells, Skeletal muscle
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-45757DOI: 10.1016/j.exger.2004.01.005OAI: diva2:266653
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-12

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Terman, AlexeiBrunk, Ulf
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