ReviewBiochimica et biophysica acta2011
Mitochondrial longevity pathways.
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed.
- Investigating the Role of Peroxisomes in Regulating Breast Cancer Stem Cell Mechanisms.International journal of molecular sciences · 2025Article
- Nutraceuticals, Social Interaction, and Psychophysiological Influence on Pet Health and Well-Being: Focus on Dogs and Cats.Veterinary sciences · 2025Review
- The de novo design and synthesis of yeast chromosome XIII facilitates investigations on aging.Nature communications · 2024Article
- Bcl-3 regulates T cell function through energy metabolism.BMC immunology · 2023Article
- Caloric Restriction Mitigates Kidney Fibrosis in an Aged and Obese Rat Model.Antioxidants (Basel, Switzerland) · 2023Article
- The Role of Mitochondrial Dysfunction in Idiopathic Pulmonary Fibrosis: New Perspectives for a Challenging Disease.Biology · 2023Review
- Review
- Quetiapine Shortens the Lifespan ofInternational journal of molecular sciences · 2022Article
- Therapeutic Potential of Mitophagy-Inducing Microflora Metabolite, Urolithin A for Alzheimer's Disease.Nutrients · 2021Review
- Sustained mitochondrial biogenesis is essential to maintain caloric restriction-induced beige adipocytes.Metabolism: clinical and experimental · 2020Article
- Anti-Ageing Effect ofInternational journal of molecular sciences · 2020Article
- Implications of Oxidative Stress and Cellular Senescence in Age-Related Thymus Involution.Oxidative medicine and cellular longevity · 2020Review
- Drug-Induced Mitochondrial Toxicity in the Geriatric Population: Challenges and Future Directions.Biology · 2019Review
- Dietary supplementation with ketoacids protects against CKD-induced oxidative damage and mitochondrial dysfunction in skeletal muscle of 5/6 nephrectomised rats.Skeletal muscle · 2018Article
- Matrine Attenuates D-Galactose-Induced Aging-Related Behavior in MiceOxidative medicine and cellular longevity · 2018Article
- DNA Damage, DNA Repair, Aging, and Neurodegeneration.Cold Spring Harbor perspectives in medicine · 2015Review
- Current aging research in China.Protein & cell · 2015Review
- Mitochondrial DNA Damage and Diseases.F1000Research · 2015Review
- Rapamycin increases mitochondrial efficiency by mtDNA-dependent reprogramming of mitochondrial metabolism in Drosophila.Journal of cell science · 2014Article
- Metabolic control of dendritic cell activation and function: recent advances and clinical implications.Frontiers in immunology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Average lifespan has increased over the last centuries, as a consequence of medical and environmental factors, but maximal life span remains unchanged. Better understanding of the underlying mechanisms of aging and determinants of life span will help to reduce age-related morbidity and facilitate healthy aging. Extension of maximal life span is currently possible in animal models with measures such as genetic manipulations and caloric restriction (CR). CR appears to prolong life by reducing oxidative damage. Reactive oxygen species (ROS) have been proposed to cause deleterious effects on DNA, proteins, and lipids, and generation of these highly reactive molecules takes place in the mitochondria. But ROS is positively implicated in cellular stress defense mechanisms and formation of ROS a highly regulated process controlled by a complex network of intracellular signaling pathways. There are endogenous anti-oxidant defense systems that have the potential to partially counteract ROS impact. In this review, we will describe pathways contributing to the regulation of the age-related decline in mitochondrial function and their impact on longevity. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.
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What OpenQuestion holds
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.