ArticleExperimental brain research2014
Protective effects of melatonin against mitochondrial injury in a mouse model of multiple sclerosis.
Article in Experimental brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The effects of melatonin supplementation on neurobehavioral outcomes and clinical severity in rodent models of multiple sclerosis; a systematic review and meta-analysis.Inflammopharmacology · 2024Pooled it
- Alpha-mangostin Ameliorates Apoptosis, Inflammation and Oxidative Stress in Cuprizone-induced Demyelination in C57BL/6 Mice.Basic and clinical neuroscience · 2025Article
- Melatonin ameliorates astrogliosis and microgliosis in a cuprizone demyelinating mouse model.Biochemistry and biophysics reports · 2025Article
- FKBP5 activates mitophagy by ablating PPAR-γ to shape a benign remyelination environment.Cell death & disease · 2023Article
- Influence of hormones in multiple sclerosis: focus on the most important hormones.Metabolic brain disease · 2023Review
- Article
- Melatonin signalling in Schwann cells during neuroregeneration.Frontiers in cell and developmental biology · 2022Review
- Mesenchymal Stem Cells Ameliorate Cuprizone-Induced Demyelination by Targeting Oxidative Stress and Mitochondrial Dysfunction.Cellular and molecular neurobiology · 2021Article
- Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases.Biomolecules · 2020Review
- Neuroprotective Effects of Melatonin during Demyelination and Remyelination Stages in a Mouse Model of Multiple Sclerosis.Journal of molecular neuroscience : MN · 2020Article
- Differential Susceptibility and Vulnerability of Brain Cells in C57BL/6 Mouse to Mitochondrial Dysfunction Induced by Short-Term Cuprizone Exposure.Frontiers in neuroanatomy · 2020Article
- Clinical relevance of circadian melatonin release in relapsing-remitting multiple sclerosis.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Melatonin and Multiple Sclerosis: From Plausible Neuropharmacological Mechanisms of Action to Experimental and Clinical Evidence.Clinical drug investigation · 2019Review
- Oligoprotective effect of metformin through the AMPK-dependent on restoration of mitochondrial hemostasis in the cuprizone-induced multiple sclerosis model.Journal of molecular histology · 2019Article
- Ameliorative effects ofAnatomy & cell biology · 2018Article
- Neuroprotective Effects of Melatonin on Experimental Allergic Encephalomyelitis Mice Via Anti-Oxidative Stress Activity.Journal of molecular neuroscience : MN · 2018Article
- Pineal Calcification, Melatonin Production, Aging, Associated Health Consequences and Rejuvenation of the Pineal Gland.Molecules (Basel, Switzerland) · 2018Review
- Melatonin as a mitochondria-targeted antioxidant: one of evolution's best ideas.Cellular and molecular life sciences : CMLS · 2017Review
- Protective effects of erythropoietin against cuprizone-induced oxidative stress and demyelination in the mouse corpus callosum.Iranian journal of basic medical sciences · 2017Article
- Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics.International journal of molecular sciences · 2016Review
Corrections and comments
- Retraction · 2023-08-07Duplication of/in Image · Manipulation of Images · Original Data and/or Images not Provided and/or not Available · Unreliable Data ·
- Retracted
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is the most prevalent inflammatory demyelinating disease of the central nervous system. Besides other pathophysiological mechanisms, mitochondrial injury is crucially involved in the development and progression of this disease. Mitochondria have been identified as targets for the peptide hormone melatonin. In the present study, we sought to evaluate the impact of oxidative stress on mitochondrial density and enzyme transcription during experimentally induced demyelination and the protective influence of melatonin. Adult male mice were fed with cuprizone for 5 weeks which caused severe demyelination of the corpus callosum (CC). Animals were simultaneously treated with melatonin by daily intra-peritoneal injections. Melatonin exposure reversed cuprizone-induced demyelination and axon protection. Transmission electron microscopy demonstrated significantly increased mitochondrial numbers and slightly increased mitochondrial size within CC axons after cuprizone exposure. Melatonin antagonized these effects and, in addition, induced the expression of subunits of the respiratory chain complex over normal control values reflecting a mechanism to compensate cuprizone-mediated down-regulation of these genes. Similarly, melatonin modulated gene expression of mitochondrial fusion and fission proteins. Biochemical analysis showed that oxidative stress induced by cuprizone was regulated by melatonin. The data implicate that melatonin abolishes destructive cuprizone effects in the CC by decreasing oxidative stress, restoring mitochondrial respiratory enzyme activity and fusion and fission processes as well as decreasing intra-axonal mitochondria accumulation.
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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.