ArticleJournal of neuroinflammation2019
Microglia lacking a peroxisomal β-oxidation enzyme chronically alter their inflammatory profile without evoking neuronal and behavioral deficits.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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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
24 citing papers in PubMed, 29 citations in OpenAlex.
- Peroxisomal integrity in demyelination-associated microglia enables cellular debris clearance and myelin renewal in mice.The Journal of clinical investigation · 2026Article
- Peroxisomes and the nervous system: progress and challenges in neuroinflammation and cell-specific functions.Frontiers in molecular neuroscience · 2026Article
- Dysregulated lipid metabolism and hypomyelination in postnatal peroxisome-deficientFrontiers in molecular neuroscience · 2026Article
- Review
- Loss of MFE-2 impairs microglial lipid homeostasis and drives neuroinflammation in Alzheimer's pathogenesis.Nature aging · 2025Article
- Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review).International journal of molecular medicine · 2025Review
- Impaired peroxisomal beta-oxidation in microglia triggers oxidative stress and impacts neurons and oligodendrocytes.Frontiers in molecular neuroscience · 2025Article
- Fundamental Neurochemistry Review: Lipids across microglial states.Journal of neurochemistry · 2025Review
- Peroxisomes as emerging clinical targets in neuroinflammatory diseases.Frontiers in molecular neuroscience · 2025Review
- The murine retinal pigment epithelium requires peroxisomal β-oxidation to maintain lysosomal function and prevent dedifferentiation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Lipid metabolism and Alzheimer's disease: clinical evidence, mechanistic link and therapeutic promise.The FEBS journal · 2023Review
- Peroxisomal defects in microglial cells induce a disease-associated microglial signature.Frontiers in molecular neuroscience · 2023Article
- Mouse Models to Study Peroxisomal Functions and Disorders: Overview, Caveats, and Recommendations.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Immune response of BV-2 microglial cells is impacted by peroxisomal beta-oxidation.Frontiers in molecular neuroscience · 2023Article
- Relationships between Inflammation and Age-Related Neurocognitive Changes.International journal of molecular sciences · 2022Review
- Dysfunctional peroxisomal lipid metabolisms and their ocular manifestations.Frontiers in cell and developmental biology · 2022Review
- Altered substrate metabolism in neurodegenerative disease: new insights from metabolic imaging.Journal of neuroinflammation · 2021Review
- Integrative iTRAQ-based proteomic and transcriptomic analysis reveals the accumulation patterns of key metabolites associated with oil quality during seed ripening of Camellia oleifera.Horticulture research · 2021Article
- Peroxisomes of the Brain: Distribution, Functions, and Associated Diseases.Neurotoxicity research · 2021Review
- Metabolic Control of Smoldering Neuroinflammation.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundMicroglia play a central role in most neurological disorders, but the impact of microgliosis on brain environment and clinical functions is not fully understood. Mice lacking multifunctional protein-2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, develop a fatal disorder characterized by motor problems similar to the milder form of MFP2 deficiency in humans. The hallmark of disease in mice is the chronic proliferation of microglia in the brain, but molecular pathomechanisms that drive rapid clinical deterioration in human and mice remain unknown. In the present study, we identified the effects of specific deletion of MFP2 from microglia in the brain on immune responses, neuronal functioning, and behavior.
methodsWe created a novel Cx3cr1-Mfp2
resultsWe found that Mfp2
conclusionOur data demonstrate that MFP2 deficiency in microglia causes intrinsic dysregulation of their inflammatory profile, which is not harmful to neuronal function, motor function, and cognition in mice during their first year of life.
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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.