ArticleThe Journal of biological chemistry2009
Reversal of the mitochondrial phenotype and slow development of oxidative biomarkers of aging in long-lived Mclk1+/- mice.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Reassessment of Genes Modulating Aging in Mice Using Demographic Measurements of the Rate of Aging.Genetics · 2018Pooled it
- Tissue-specific mitochondrial pathway remodeling linked to longevity in honeybee queens.PloS one · 2026Article
- Mammalian mitohormesis: from mitochondrial stressors to organismal benefits.The EMBO journal · 2025Review
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- Metformin modulates the unfolded protein responses, altering lifespan and health-promoting effects in UPR-activated worms.PloS one · 2025Article
- New Insights on the Uptake and Trafficking of Coenzyme Q.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Dysregulation of iron homeostasis and methamphetamine reward behaviors in Clk1-deficient mice.Acta pharmacologica Sinica · 2022Article
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- Animal Models of Coenzyme Q Deficiency: Mechanistic and Translational Learnings.Antioxidants (Basel, Switzerland) · 2021Review
- Combinatorial Approach UsingMolecules and cells · 2021Review
- Loss ofInternational journal of molecular sciences · 2021Article
- Integrating cellular senescence with the concept of damage accumulation in aging: Relevance for clearance of senescent cells.Aging cell · 2019Review
- Therapeutic Efficacy of Molecular Hydrogen: A New Mechanistic Insight.Current pharmaceutical design · 2019Review
- The Naked Mole Rat: A Unique Example of Positive Oxidative Stress.Oxidative medicine and cellular longevity · 2019Review
- Epicatechin modulates stress-resistance in C. elegans via insulin/IGF-1 signaling pathway.PloS one · 2019Article
- Reduction in the levels of CoQ biosynthetic proteins is related to an increase in lifespan without evidence of hepatic mitohormesis.Scientific reports · 2018Article
- Mitochondrial ubiquinone-mediated longevity is marked by reduced cytoplasmic mRNA translation.Life science alliance · 2018Article
- Lifelong reduction in complex IV induces tissue-specific metabolic effects but does not reduce lifespan or healthspan in mice.Aging cell · 2018Article
- Subcellular Redox Targeting: Bridging in Vitro and in Vivo Chemical Biology.ACS chemical biology · 2017Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although there is a consensus that mitochondrial function is somehow linked to the aging process, the exact role played by mitochondria in this process remains unresolved. The discovery that reduced activity of the mitochondrial enzyme CLK-1/MCLK1 (also known as COQ7) extends lifespan in both Caenorhabditis elegans and mice has provided a genetic model to test mitochondrial theories of aging. We have recently shown that the mitochondria of young, long-lived, Mclk1(+/-) mice are dysfunctional, exhibiting reduced energy metabolism and a substantial increase in oxidative stress. Here we demonstrate that this altered mitochondrial condition in young animals paradoxically results in an almost complete protection from the age-dependent loss of mitochondrial function as well as in a significant attenuation of the rate of development of oxidative biomarkers of aging. Moreover, we show that reduction in MCLK1 levels can also gradually prevent the deterioration of mitochondrial function and associated increase of global oxidative stress that is normally observed in Sod2(+/-) mutants. We hypothesize that the mitochondrial dysfunction observed in young Mclk1(+/-) mutants induces a physiological state that ultimately allows for their slow rate of aging. Thus, our study provides for a unique vertebrate model in which an initial alteration in a specific mitochondrial function is linked to long term beneficial effects on biomarkers of aging and, furthermore, provides for new evidence which indicates that mitochondrial oxidative stress is not causal to aging.
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