Mitochondrial damage and intralysosomal degradation in cellular aging
2006 (English)In: Molecular Aspects of Medicine, ISSN 0098-2997, Vol. 27, no 5-6, 471-482 p.Article in journal (Refereed) Published
Normal mitochondrial respiration is associated with a continuous production of superoxide and hydrogen peroxide, inevitably resulting in minor macromolecular damage. Damaged cellular components are not completely turned over by autophagy and other cellular repair systems, leading to a progressive age-related accumulation of biological "garbage" material, such as defective mitochondria, cytoplasmic protein aggregates and an intralysosomal undegradable material, lipofuscin. These changes primarily affect neurons, cardiac myocytes and other long-lived postmitotic cells that neither dilute this "garbage" by mitotic activity, nor are replaced by newly differentiated cells. Defective mitochondria are insufficient in ATP production and often generate increased amounts of reactive oxygen species, further enhancing oxidative stress. Lipofuscin-loaded lysosomes, in turn, poorly turn over mitochondria that gradually leads to the overload of long-lived postmitotic cells with "garbage" material, decreased adaptability and eventual cell death. © 2006 Elsevier Ltd. All rights reserved.
Place, publisher, year, edition, pages
2006. Vol. 27, no 5-6, 471-482 p.
Aging; Autophagocytosis; Lysosomes; Mitochondria; Oxidative stress
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-36022DOI: 10.1016/j.mam.2006.08.006Local ID: 29446OAI: oai:DiVA.org:liu-36022DiVA: diva2:256870