Cited by 149Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsMuscle Physiology and Disorders

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Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle

Hütter, Eveline, Skovbro, Mette, Lener, Barbara, Prats, Clara, Rabøl, Rasmus, Dela, Flemming, Jansen‐Dürr, Pidder·2007·Aging Cell

DOI 10.1111/j.1474-9726.2007.00282.x

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Abstract

Summary: According to the free radical theory of aging, reactive oxygen species (ROS) act as a driving force of the aging process, and it is generally believed that mitochondrial dysfunction is a major source of increased oxidative stress in tissues with high content of mitochondria, such as muscle or brain. However, recent experiments in mouse models of premature aging have questioned the role of mitochondrial ROS production in premature aging. To address the role of mitochondrial impairment and ROS production for aging in human muscles, we have analyzed mitochondrial properties in muscle fibres isolated from the vastus lateralis of young and elderly donors. Mitochondrial respiratory functions were addressed by high‐resolution respirometry, and ROS production was analyzed by in situ staining with the redox‐sensitive dye dihydroethidium. We found that aged human skeletal muscles contain fully functional mitochondria and that the level of ROS production is higher in young compared to aged muscle. Accordingly, we could not find any increase in oxidative modification of proteins in muscle from elderly donors. However, the accumulation of lipofuscin was identified as a robust marker of human muscle aging. The data support a model, where ROS‐induced molecular damage is continuously removed, preventing the accumulation of dysfunctional mitochondria despite ongoing ROS production.

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Authors: Hütter, E., Skovbro, M., Lener, B., Prats, C., Rabøl, R., Dela, F., & Jansen‐Dürr, P.
Affiliations: Austrian Academy of Sciences (AT)
University of Copenhagen (DK)
ORCID: Prats, Clara
Dela, Flemming
Jansen‐Dürr, Pidder
Venue: Aging Cell
Publisher: Wiley
Published: 2007-02-05
Volume: 6
Issue: 2
Pages: 245-256
ISSN: 1474-9718 (ISSN-L)
1474-9726
DOI: 10.1111/j.1474-9726.2007.00282.x
OpenAlex: W2007891985
Cited by: 149
References: 52
Citations by year: 2026: 2 · 2025: 3 · 2024: 13 · 2023: 7 · 2022: 5 · 2021: 8 · 2020: 6 · 2019: 8 · 2018: 6 · 2017: 10 · 2016: 13 · 2015: 11 · 2014: 10 · 2013: 8 · 2012: 10
FWCI: 3.44
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Aging Cell (publishedVersion)
PubMed (publishedVersion)
Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords: muscle aging, oxidative stress, reactive oxygen species, mitochondrial dysfunction, lipofuscin accumulation, skeletal muscle, mitochondrial respiration, protein oxidative modification, free radical theory of aging, vastus lateralis, mitochondrial quality control
MeSH terms: Adult, Aged, Aging, Biopsy, Female, Humans, Lipofuscin, Male, Mitochondria, Oxygen Consumption, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal, Cell Respiration

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Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle

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