Lipofuscin: Mechanisms of formation and increase with age
Identifieur interne : 002814 ( Main/Exploration ); précédent : 002813; suivant : 002815Lipofuscin: Mechanisms of formation and increase with age
Auteurs : Alexei Terman [Suède, Ukraine] ; Ulf T. Brunk [Suède]Source :
- APMIS [ 0903-4641 ] ; 1998-01.
English descriptors
- Teeft :
- Academic press, Accumulation, Acidic vacuolar apparatus, Acta neuropathol, Ageing, Autofluorescent inclusions, Autophagic vacuoles, Autophagocytosed material, Autophagocytosis, Autophagocytotic degradation, Biochemical studies, Biol, Brain cells, Brain neurons, Brain regions, Brunk, Caloric restriction, Cardiac, Cardiac lipofuscin, Cardiac myocytes, Cathepsin, Cell biol, Cell components, Cell cultures, Cerebrospinal fluid, Ceroid, Ceroid accumulation, Ceroid formation, Cultured, Cultured cells, Degradation, Dense bodies, Different ages, Different types, Electron microsc, Exact mechanisms, Excerpta medica, Exocytosis, Experimental studies, Ferrous iron, Free radicals, Gerontol, Gerontology, Glial cells, Granule, Heart myocytes, Hepatocytes, Heterophagocytosed material, Hydrogen peroxide, Inclusion, Inhibitor, Intracellular, Intracellular degradation, Intracellular protein degradation, Intralysosomal, Intralysosomal degradation, Intralysosomal material, Leupeptin, Leupeptin causes, Leupeptin treatment, Lipid, Lipid peroxidation products, Lipofuscin, Lipofuscin accumulation, Lipofuscin formation, Lipofuscin granules, Lipofuscin pigment accumulation, Lipofuscinogenesis, Liver lysosomes, Lysosomal, Lysosomal degradative capacity, Lysosomal enzymes, Lysosomal function, Lysosomal functions, Lysosomal storage diseases, Lysosome, Mech, Microglial cells, Mononuclear phagocytes, Morphometric analysis, Myocytes, Neuron, Neuronal, Neuronal ceroid lipofuscinosis, Numerous studies, Other lysosomes, Oxidative, Oxidative reactions, Oxidative stress, Oxygen tension, Pathol, Peroxidation, Pigment, Pigment accumulation, Pigment formation, Pigment research, Possible mechanisms, Postmitotic, Postmitotic cells, Present knowledge, Protease, Protective effect, Protein modification, Reactive oxygen species, Residual bodies, Retinal pigment epithelial cells, Retinal pigment epithelium, Secondary lysosomes, Similar effect, Skeletal muscle cells, Sohal, Special reference, Such cells, Terman, Terman brunk, Virchows arch, Young rats.
Abstract
Lipofuscin (age pigment) is a brown‐yellow, electron‐dense, autofluorescent material that accumulates progressively over time in lysosomes of postmitotic cells, such as neurons and cardiac myocytes. The exact mechanisms behind this accumulation are still unclear. This review outlines the present knowledge of age pigment formation, and considers possible mechanisms responsible for the increase of lipofuscin with age. Numerous studies indicate that the formation of lipofuscin is due to the oxidative alteration of macromolecules by oxygen‐derived free radicals generated in reactions catalyzed by redox‐active iron of low molecular weight. Two principal explanations for the increase of lipofuscin with age have been suggested. The first one is based on the notion that lipofuscin is not totally eliminated (either by degradation or exocytosis) even at young age, and, thus, accumulates in postmitotic cells as a function of time. Since oxidative reactions are obligatory for life, they would act as age‐independent enhancers of lipofuscin accumulation, as well as of many other manifestations of senescence. The second explanation is that the increase of lipofuscin is an effect of aging, caused by an age‐related enhancement of autophagocytosis, a decline in intralysosomal degradation, and/or a decrease in exocytosis.
Url:
DOI: 10.1111/j.1699-0463.1998.tb01346.x
Affiliations:
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Brunk</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Pathology II, Faculty of Health Sciences, Linköping University, Linköping</wicri:regionArea><wicri:noRegion>Linköping</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">APMIS</title><title level="j" type="alt">APMIS</title><idno type="ISSN">0903-4641</idno><idno type="eISSN">1600-0463</idno><imprint><biblScope unit="vol">106</biblScope><biblScope unit="issue">1‐6</biblScope><biblScope unit="page" from="265">265</biblScope><biblScope unit="page" to="276">276</biblScope><biblScope unit="page-count">12</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-01">1998-01</date></imprint><idno type="ISSN">0903-4641</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0903-4641</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Academic press</term><term>Accumulation</term><term>Acidic vacuolar apparatus</term><term>Acta neuropathol</term><term>Ageing</term><term>Autofluorescent inclusions</term><term>Autophagic vacuoles</term><term>Autophagocytosed material</term><term>Autophagocytosis</term><term>Autophagocytotic degradation</term><term>Biochemical studies</term><term>Biol</term><term>Brain cells</term><term>Brain neurons</term><term>Brain regions</term><term>Brunk</term><term>Caloric restriction</term><term>Cardiac</term><term>Cardiac lipofuscin</term><term>Cardiac myocytes</term><term>Cathepsin</term><term>Cell biol</term><term>Cell components</term><term>Cell cultures</term><term>Cerebrospinal fluid</term><term>Ceroid</term><term>Ceroid accumulation</term><term>Ceroid formation</term><term>Cultured</term><term>Cultured cells</term><term>Degradation</term><term>Dense bodies</term><term>Different ages</term><term>Different types</term><term>Electron microsc</term><term>Exact mechanisms</term><term>Excerpta medica</term><term>Exocytosis</term><term>Experimental studies</term><term>Ferrous iron</term><term>Free radicals</term><term>Gerontol</term><term>Gerontology</term><term>Glial cells</term><term>Granule</term><term>Heart myocytes</term><term>Hepatocytes</term><term>Heterophagocytosed material</term><term>Hydrogen peroxide</term><term>Inclusion</term><term>Inhibitor</term><term>Intracellular</term><term>Intracellular degradation</term><term>Intracellular protein degradation</term><term>Intralysosomal</term><term>Intralysosomal degradation</term><term>Intralysosomal material</term><term>Leupeptin</term><term>Leupeptin causes</term><term>Leupeptin treatment</term><term>Lipid</term><term>Lipid peroxidation products</term><term>Lipofuscin</term><term>Lipofuscin accumulation</term><term>Lipofuscin formation</term><term>Lipofuscin granules</term><term>Lipofuscin pigment accumulation</term><term>Lipofuscinogenesis</term><term>Liver lysosomes</term><term>Lysosomal</term><term>Lysosomal degradative capacity</term><term>Lysosomal enzymes</term><term>Lysosomal function</term><term>Lysosomal functions</term><term>Lysosomal storage diseases</term><term>Lysosome</term><term>Mech</term><term>Microglial cells</term><term>Mononuclear phagocytes</term><term>Morphometric analysis</term><term>Myocytes</term><term>Neuron</term><term>Neuronal</term><term>Neuronal ceroid lipofuscinosis</term><term>Numerous studies</term><term>Other lysosomes</term><term>Oxidative</term><term>Oxidative reactions</term><term>Oxidative stress</term><term>Oxygen tension</term><term>Pathol</term><term>Peroxidation</term><term>Pigment</term><term>Pigment accumulation</term><term>Pigment formation</term><term>Pigment research</term><term>Possible mechanisms</term><term>Postmitotic</term><term>Postmitotic cells</term><term>Present knowledge</term><term>Protease</term><term>Protective effect</term><term>Protein modification</term><term>Reactive oxygen species</term><term>Residual bodies</term><term>Retinal pigment epithelial cells</term><term>Retinal pigment epithelium</term><term>Secondary lysosomes</term><term>Similar effect</term><term>Skeletal muscle cells</term><term>Sohal</term><term>Special reference</term><term>Such cells</term><term>Terman</term><term>Terman brunk</term><term>Virchows arch</term><term>Young rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lipofuscin (age pigment) is a brown‐yellow, electron‐dense, autofluorescent material that accumulates progressively over time in lysosomes of postmitotic cells, such as neurons and cardiac myocytes. The exact mechanisms behind this accumulation are still unclear. This review outlines the present knowledge of age pigment formation, and considers possible mechanisms responsible for the increase of lipofuscin with age. Numerous studies indicate that the formation of lipofuscin is due to the oxidative alteration of macromolecules by oxygen‐derived free radicals generated in reactions catalyzed by redox‐active iron of low molecular weight. Two principal explanations for the increase of lipofuscin with age have been suggested. The first one is based on the notion that lipofuscin is not totally eliminated (either by degradation or exocytosis) even at young age, and, thus, accumulates in postmitotic cells as a function of time. Since oxidative reactions are obligatory for life, they would act as age‐independent enhancers of lipofuscin accumulation, as well as of many other manifestations of senescence. The second explanation is that the increase of lipofuscin is an effect of aging, caused by an age‐related enhancement of autophagocytosis, a decline in intralysosomal degradation, and/or a decrease in exocytosis.</div></front></TEI><affiliations><list><country><li>Suède</li><li>Ukraine</li></country></list><tree><country name="Suède"><noRegion><name sortKey="Terman, Alexei" sort="Terman, Alexei" uniqKey="Terman A" first="Alexei" last="Terman">Alexei Terman</name></noRegion><name sortKey="Brunk, Ulf T" sort="Brunk, Ulf T" uniqKey="Brunk U" first="Ulf T." last="Brunk">Ulf T. Brunk</name><name sortKey="Terman, Alexei" sort="Terman, Alexei" uniqKey="Terman A" first="Alexei" last="Terman">Alexei Terman</name></country><country name="Ukraine"><noRegion><name sortKey="Terman, Alexei" sort="Terman, Alexei" uniqKey="Terman A" first="Alexei" last="Terman">Alexei Terman</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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