ArticleAging cell2014
Lifelong treatment with atenolol decreases membrane fatty acid unsaturation and oxidative stress in heart and skeletal muscle mitochondria and improves immunity and behavior, without changing mice longevity.
Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Atenolol is associated with salivary gland dysfunction and sialochemical alterations, along with redox imbalance and structural changes in male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Atenolol Ameliorates Skeletal Muscle Atrophy and Oxidative Stress Induced by Cast Immobilization in Rats.Biomedicines · 2023Article
- Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.International journal of molecular sciences · 2022Review
- Review
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- The Advanced Lipoxidation End-Product Malondialdehyde-Lysine in Aging and Longevity.Antioxidants (Basel, Switzerland) · 2020Review
- The value of serum metabolomics analysis in predicting the response to cardiac resynchronization therapy.Journal of geriatric cardiology : JGC · 2019Article
- Mitochondria in β-adrenergic signaling: emerging therapeutic perspectives in heart failure and ventricular arrhythmias.Journal of thoracic disease · 2018Article
- Mitochondrial DNA levels in Huntington disease leukocytes and dermal fibroblasts.Metabolic brain disease · 2017Article
- Impaired cardiac and skeletal muscle bioenergetics in children, adolescents, and young adults with Barth syndrome.Physiological reports · 2017Article
- Analysis of Serum Metabolites to Diagnose Bicuspid Aortic Valve.Scientific reports · 2016Article
- Reconsidering the Role of Mitochondria in Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2015Review
- Mitochondrial dysfunction in cardiac aging.Biochimica et biophysica acta · 2015Review
- The influence of dietary fat source on liver and skeletal muscle mitochondrial modifications and lifespan changes in calorie-restricted mice.Biogerontology · 2015Review
- Cysteine dietary supplementation reverses the decrease in mitochondrial ROS production at complex I induced by methionine restriction.Journal of bioenergetics and biomembranes · 2015Article
- Target of rapamycin activation predicts lifespan in fruit flies.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane fatty acid unsaturation hypothesis of aging and longevity is experimentally tested for the first time in mammals. Lifelong treatment of mice with the β1-blocker atenolol increased the amount of the extracellular-signal-regulated kinase signaling protein and successfully decreased one of the two traits appropriately correlating with animal longevity, the membrane fatty acid unsaturation degree of cardiac and skeletal muscle mitochondria, changing their lipid profile toward that present in much more longer-lived mammals. This was mainly due to decreases in 22:6n-3 and increases in 18:1n-9 fatty acids. The atenolol treatment also lowered visceral adiposity (by 24%), decreased mitochondrial protein oxidative, glycoxidative, and lipoxidative damage in both organs, and lowered oxidative damage in heart mitochondrial DNA. Atenolol also improved various immune (chemotaxis and natural killer activities) and behavioral functions (equilibrium, motor coordination, and muscular vigor). It also totally or partially prevented the aging-related detrimental changes observed in mitochondrial membrane unsaturation, protein oxidative modifications, and immune and behavioral functions, without changing longevity. The controls reached 3.93 years of age, a substantially higher maximum longevity than the best previously described for this strain (3.0 years). Side effects of the drug could have masked a likely lowering of the endogenous aging rate induced by the decrease in membrane fatty acid unsaturation. We conclude that it is atenolol that failed to increase longevity, and likely not the decrease in membrane unsaturation induced by the drug.
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