ArticleCirculation2009
Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging.
Article in Circulation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 302 papers, 1 of them a synthesis that pooled it.
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Who cites it
302 citing papers in PubMed, 1 synthesis or guideline pooled it, 487 citations in OpenAlex.
- Unveiling the Mechanism of Protective Effects of Tanshinone as a New Fighter Against Cardiovascular Diseases: A Systematic Review.Cardiovascular toxicology · 2024Pooled it
- Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.Basic research in cardiology · 2026Article
- Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age.bioRxiv : the preprint server for biology · 2026Article
- USP18 Serves as a Key Mediator of cGAS-STING for Cardiac Aging in Diabetes.Cell biochemistry and function · 2026Article
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Bench to bedside: is rapamycin headed for the docTOR?GeroScience · 2026Review
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Late-in-life treadmill training mitigates gut microbiome imbalances and cardiovascular disease risk in mice.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Irradiation-induced brain senescence accelerates cardiac aging via systemic mechanisms: insights from transcriptomic profiling.GeroScience · 2026Article
- Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Aging: Current Insights and Therapeutic Advances.Biomedicines · 2026Review
- Severely reduced antioxidant and impaired mitochondrial biomarkers could be linked to post-tuberculosis lung disease in a cohort from South Africa.African journal of thoracic and critical care medicine · 2026Article
- Regulation of stem cell aging and cellular proliferation by Klotho-Sirt1 pathways in heart, kidney and small intestine.npj aging · 2025Article
- The Human Cardiac "Age-OME": Age-Specific Changes in Myocardial Molecular Expression.Aging cell · 2025Article
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Cellular Models of Aging and Senescence.Cells · 2025Review
- Article
- Cardiac Damage in Hypertension: From Molecular Mechanisms to Novel Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Article
- Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
242 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAge is a major risk for cardiovascular diseases. Although mitochondrial reactive oxygen species have been proposed as one of the causes of aging, their role in cardiac aging remains unclear. We have previously shown that overexpression of catalase targeted to mitochondria (mCAT) prolongs murine median lifespan by 17% to 21%. METHODS AND
resultsWe used echocardiography to study cardiac function in aging cohorts of wild-type and mCAT mice. Changes found in wild-type mice recapitulate human aging: age-dependent increases in left ventricular mass index and left atrial dimension, worsening of the myocardial performance index, and a decline in diastolic function. Cardiac aging in mice is accompanied by accumulation of mitochondrial protein oxidation, increased mitochondrial DNA mutations and deletions and mitochondrial biogenesis, increased ventricular fibrosis, enlarged myocardial fiber size, decreased cardiac SERCA2 protein, and activation of the calcineurin-nuclear factor of activated T-cell pathway. All of these age-related changes were significantly attenuated in mCAT mice. Analysis of survival of 130 mice demonstrated that echocardiographic cardiac aging risk scores were significant predictors of mortality. The estimated attributable risk to mortality for these 2 parameters was 55%.
conclusionsThis study shows that cardiac aging in the mouse closely recapitulates human aging and demonstrates the critical role of mitochondrial reactive oxygen species in cardiac aging and the impact of cardiac aging on survival. These findings also support the potential application of mitochondrial antioxidants in reactive oxygen species-related cardiovascular diseases.
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Registered trials
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