ArticleAging cell2016
Mitochondrial-targeted catalase is good for the old mouse proteome, but not for the young: 'reverse' antagonistic pleiotropy?
Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 40 citations in OpenAlex.
- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- The Role of Molecular and Cellular Aging Pathways on Age-Related Hearing Loss.International journal of molecular sciences · 2024Review
- Mitochondrial Oxidative Stress Regulates FOXP3+ T-Cell Activity and CD4-Mediated Inflammation in Older Adults with Frailty.International journal of molecular sciences · 2024Article
- Mitochondria-Targeted Catalase Does Not Suppress Development of Cellular Senescence during Aging.Biomedicines · 2024Article
- Identification and functional analysis of senescent cells in the cardiovascular system using omics approaches.American journal of physiology. Heart and circulatory physiology · 2023Review
- The transcription regulator ATF4 is a mediator of skeletal muscle aging.GeroScience · 2023Article
- TurnoveR: A Skyline External Tool for Analysis of Protein Turnover in Metabolic Labeling Studies.Journal of proteome research · 2023Article
- Proteomes of primary skin fibroblasts from healthy individuals reveal altered cell responses across the life span.Aging cell · 2022Article
- Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry.Journal of visualized experiments : JoVE · 2022Article
- Altering aspects of mitochondrial quality to improve musculoskeletal outcomes in disuse atrophy.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Methylation-dependent antioxidant-redox imbalance regulates hypertensive kidney injury in aging.Redox biology · 2020Article
- Enhanced Expression of Catalase in Mitochondria Modulates NF-κB-Dependent Lung Inflammation through Alteration of Metabolic Activity in Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Targeting reactive oxygen species (ROS) to combat the age-related loss of muscle mass and function.Biogerontology · 2020Review
- Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice.eLife · 2020Article
- Proteomics of Long-Lived Mammals.Proteomics · 2020Review
- Accumulation of "Old Proteins" and the Critical Need for MS-based Protein Turnover Measurements in Aging and Longevity.Proteomics · 2020Review
- Function, Oxidative, and Inflammatory Stress Parameters in Immune Cells as Predictive Markers of Lifespan throughout Aging.Oxidative medicine and cellular longevity · 2019Article
- Protein synthesis and quality control in aging.Aging · 2018Review
- Balance of cardiac and systemic hepcidin and its role in heart physiology and pathology.Laboratory investigation; a journal of technical methods and pathology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules associated with aging and a broad spectrum of pathologies. We have previously shown that transgenic expression of the antioxidant enzyme catalase targeted to the mitochondria (mCAT) in mice reduces ROS, attenuates age-related disease, and increases lifespan. However, it has been increasingly recognized that ROS also has beneficial roles in signaling, hormesis, stress response, and immunity. We therefore hypothesized that mCAT might be beneficial only when ROS approaches pathological levels in older age and might not be advantageous at a younger age when basal ROS is low. We analyzed abundance and turnover of the global proteome in hearts and livers of young (4 month) and old (20 month) mCAT and wild-type (WT) mice. In old hearts and livers of WT mice, protein half-lives were reduced compared to young, while in mCAT mice the reverse was observed; the longest half-lives were seen in old mCAT mice and the shortest in young mCAT. Protein abundance of old mCAT hearts recapitulated a more youthful proteomic expression profile (P-value < 0.01). However, young mCAT mice partially phenocopied the older wild-type proteome (P-value < 0.01). Age strongly interacts with mCAT, consistent with antagonistic pleiotropy in the reverse of the typical direction. These findings underscore the contrasting roles of ROS in young vs. old mice and indicate the need for better understanding of the interaction between dose and age in assessing the efficacy of therapeutic interventions in aging, including mitochondrial antioxidants.
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