ArticleFree radical biology & medicine2007
Age-related increases in oxidatively damaged proteins of mouse kidney mitochondrial electron transport chain complexes.
Article in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed.
- Small-scale protocols to characterize mitochondrial Complex V activity and assembly in peripheral blood mononuclear cells.PloS one · 2025Article
- Oxidative Stress Promotes Axonal Atrophy through Alterations in Microtubules and EB1 Function.Aging and disease · 2024Article
- Maternal Low-Protein Diet Leads to Mitochondrial Dysfunction and Impaired Energy Metabolism in the Skeletal Muscle of Male Rats.International journal of molecular sciences · 2024Article
- Molecular Mechanisms Associated with Aging Kidneys and Future Perspectives.International journal of molecular sciences · 2023Review
- Light, Water, and Melatonin: The Synergistic Regulation of Phase Separation in Dementia.International journal of molecular sciences · 2023Review
- Advances in Postharvest Storage and Preservation Strategies forFoods (Basel, Switzerland) · 2023Review
- Uremic Myopathy and Mitochondrial Dysfunction in Kidney Disease.International journal of molecular sciences · 2022Article
- Targeting ER stress and calpain activation to reverse age-dependent mitochondrial damage in the heart.Mechanisms of ageing and development · 2020Review
- Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats.Aging · 2020Article
- A Therapeutic Connection between Dietary Phytochemicals and ATP Synthase.Current medicinal chemistry · 2017Review
- Aldehyde dehydrogenase 2 activation and coevolution of its εPKC-mediated phosphorylation sites.Journal of biomedical science · 2017Article
- The Role of Mitochondrial Aldehyde Dehydrogenase 2 (ALDH2) in Neuropathology and Neurodegeneration.Acta neurologica Taiwanica · 2016Review
- Malondialdehyde Epitopes as Targets of Immunity and the Implications for Atherosclerosis.Advances in immunology · 2016Review
- Article
- Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera).Age (Dordrecht, Netherlands) · 2013Article
- Association between age-related decline of kidney function and plasma malondialdehyde.Rejuvenation research · 2012Article
- Ischemic preconditioning: the role of mitochondria and aging.Experimental gerontology · 2012Review
- Review
- Article
- Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.PloS one · 2011Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mitochondrial dysfunction generates reactive oxygen species (ROS) which damage essential macromolecules. Oxidative modification of proteins, DNA, and lipids has been implicated as a major causal factor in the age-associated decline in tissue function. Mitochondrial electron transport chain complexes I and III are the principal sites of ROS production, and oxidative modifications to the complex subunits inhibit their in vitro activity. Therefore, we hypothesize that mitochondrial complex subunits may be primary targets for oxidative damage by ROS which may impair normal complex activity by altering their structure/function leading to mitochondrial dysfunction associated with aging. This study of kidney mitochondria from young, middle-aged, and old mice reveals that there are functional decreases in complexes I, II, IV, and V between aged compared to young kidney mitochondria and these functional declines directly correlate with increased oxidative modification to particular complex subunits. We postulate that the electron leakage from complexes causes specific damage to their subunits and increased ROS generation as oxidative damage accumulates, leading to further mitochondrial dysfunction, a cyclical process that underlies the progressive decline in physiologic function seen in aged mouse kidney. In conclusion, increasing mitochondrial dysfunction may play a key role in the age-associated decline in tissue function.
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Registered trials
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