ArticleFree radical biology & medicine2008
Age-related alterations in oxidatively damaged proteins of mouse heart mitochondrial electron transport chain complexes.
Article in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 72 citations in OpenAlex.
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Endometrial Aging and Reproductive Decline: The Central Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- Expression of mitochondrial oxidative stress response genes in muscle is associated with mitochondrial respiration, physical performance, and muscle mass in the Study of Muscle, Mobility and Aging (SOMMA).medRxiv : the preprint server for health sciences · 2023Article
- Article
- Dietary MgInternational journal of molecular sciences · 2020Article
- Effects of aging and exercise training on mitochondrial function and apoptosis in the rat heart.Pflugers Archiv : European journal of physiology · 2020Article
- Article
- Effect of Aging on Mitochondrial Energetics in the Human Atria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats.Journal of molecular and cellular cardiology · 2014Article
- Inhibition of delta-6 desaturase reverses cardiolipin remodeling and prevents contractile dysfunction in the aged mouse heart without altering mitochondrial respiratory function.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
- A comprehensive study of myocardial redox homeostasis in naturally and mimetically aged rats.Age (Dordrecht, Netherlands) · 2014Article
- Age-dependent mitochondrial energy dynamics in the mice heart: role of superoxide dismutase-2.Experimental gerontology · 2013Article
- Age-related differences in cardiac ischemia-reperfusion injury: effects of estrogen deficiency.Pflugers Archiv : European journal of physiology · 2013Review
- Reduced mitochondrial ROS, enhanced antioxidant defense, and distinct age-related changes in oxidative damage in muscles of long-lived Peromyscus leucopus.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Aging-dependent changes in rat heart mitochondrial glutaredoxins--Implications for redox regulation.Redox biology · 2013Article
- A comparative 'bottom up' proteomics strategy for the site-specific identification and quantification of protein modifications by electrophilic lipids.Journal of proteomics · 2012Article
- Age-related decline in mitochondrial bioenergetics: does supercomplex destabilization determine lower oxidative capacity and higher superoxide production?Seminars in cell & developmental biology · 2012Review
- Age-dependent reductions in mitochondrial respiration are exacerbated by calcium in the female rat heart.Gender medicine · 2012Article
- Effect of lifestyle on age-related mitochondrial protein oxidation in mice cardiac muscle.European journal of applied physiology · 2012Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrially generated ROS increase with age and are a major factor that damages proteins by oxidative modification. Accumulation of oxidatively damaged proteins has been implicated as a causal factor in the age-associated decline in tissue function. Mitochondrial electron transport chain (ETC) complexes I and III are the principle sites of ROS production, and oxidative modifications to their complex subunits inhibit their in vitro activity. We hypothesize that mitochondrial complex subunits may be primary targets for modification by ROS, which may impair normal complex activity. This study of heart mitochondria from young, middle-aged, and old mice reveals that there is an age-related decline in complex I and V activity that correlates with increased oxidative modification to their subunits. The data also show a specificity for modifications of the ETC complex subunits, i.e., several proteins have more than one type of adduct. We postulate that the electron leakage from ETC 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 of the aged mouse heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.