ArticlePloS one2012
Long-term bezafibrate treatment improves skin and spleen phenotypes of the mtDNA mutator mouse.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Exercise mimetics: molecular mechanisms, biological and therapeutic effects.Molecular biomedicine · 2026Review
- Lipodystrophy in methylmalonic acidemia associated with elevated FGF21 and abnormal methylmalonylation.JCI insight · 2024Article
- Emerging Multi-omic Approaches to the Molecular Diagnosis of Mitochondrial Disease and Available Strategies for Treatment and Prevention.Current genomics · 2024Review
- Recent advances in small molecules for improving mitochondrial disorders.RSC advances · 2023Review
- PGC-1α Is a Master Regulator of Mitochondrial Lifecycle and ROS Stress Response.Antioxidants (Basel, Switzerland) · 2023Review
- HRAS germline mutations impair LKB1/AMPK signaling and mitochondrial homeostasis in Costello syndrome models.The Journal of clinical investigation · 2022Article
- Mitochondrial DNA copy number in human disease: the more the better?FEBS letters · 2021Review
- Tocotrienol Supplementation Led to Higher Serum Levels of Lysophospholipids but Lower Acylcarnitines in Postmenopausal Women: A Randomized Double-Blinded Placebo-Controlled Clinical Trial.Frontiers in nutrition · 2021Article
- Current progress in the therapeutic options for mitochondrial disorders.Physiological research · 2020Article
- Therapeutic Approaches to Treat Mitochondrial Diseases: "One-Size-Fits-All" and "Precision Medicine" Strategies.Pharmaceutics · 2020Review
- Metabolic effects of bezafibrate in mitochondrial disease.EMBO molecular medicine · 2020Observational
- The exercise cytokine interleukin-15 rescues slow wound healing in aged mice.The Journal of biological chemistry · 2019Article
- Review
- Elucidating the Beneficial Role of PPAR Agonists in Cardiac Diseases.International journal of molecular sciences · 2018Review
- Emerging therapies for mitochondrial diseases.Essays in biochemistry · 2018Review
- The Effects of PPAR Stimulation on Cardiac Metabolic Pathways in Barth Syndrome Mice.Frontiers in pharmacology · 2018Article
- Inherited mitochondrial genomic instability and chemical exposures.Toxicology · 2017Review
- Therapies for mitochondrial diseases and current clinical trials.Molecular genetics and metabolism · 2017Review
- The PPAR pan-agonist bezafibrate ameliorates cardiomyopathy in a mouse model of Barth syndrome.Orphanet journal of rare diseases · 2017Article
- Sustained AMPK activation improves muscle function in a mitochondrial myopathy mouse model by promoting muscle fiber regeneration.Human molecular genetics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Pharmacological agents, such as bezafibrate, that activate peroxisome proliferator-activated receptors (PPARs) and PPAR γ coactivator-1α (PGC-1α) pathways have been shown to improve mitochondrial function and energy metabolism. The mitochondrial DNA (mtDNA) mutator mouse is a mouse model of aging that harbors a proofreading-deficient mtDNA polymerase γ. These mice develop many features of premature aging including hair loss, anemia, osteoporosis, sarcopenia and decreased lifespan. They also have increased mtDNA mutations and marked mitochondrial dysfunction. We found that mutator mice treated with bezafibrate for 8-months had delayed hair loss and improved skin and spleen aging-like phenotypes. Although we observed an increase in markers of fatty acid oxidation in these tissues, we did not detect a generalized increase in mitochondrial markers. On the other hand, there were no improvements in muscle function or lifespan of the mutator mouse, which we attributed to the rodent-specific hepatomegaly associated with fibrate treatment. These results showed that despite its secondary effects in rodent's liver, bezafibrate was able to improve some of the aging phenotypes in the mutator mouse. Because the associated hepatomegaly is not observed in primates, long-term bezafibrate treatment in humans could have beneficial effects on tissues undergoing chronic bioenergetic-related degeneration.
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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.