ArticleNPJ Regenerative medicine2024
Myeloid cell-associated aromatic amino acid metabolism facilitates CNS myelin regeneration.
Article in NPJ Regenerative medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Integrated Single-Cell and Spatial Transcriptomic Analysis Identifies Putative Metabolic Crosstalk BetweenCancers · 2026Article
- [Application of chromatography-mass spectrometry in the clinical analysis of multiple sclerosis].Se pu = Chinese journal of chromatography · 2026Review
- Metabolic signatures in sciatic nerve of PMP22 transgenic rats provide insights into the pathogenesis of charcot-marie-tooth disease type 1 A.Scientific reports · 2026Article
- Remote ischemic postconditioning improves cognitive dysfunction after subarachnoid hemorrhage by driving metabolic reprogramming of border-associated macrophages through the IL-33/ST2 axis.Journal of neuroinflammation · 2025Article
- Differential Effects of IL4I1 Protein on Lymphocytes From Healthy and Multiple Sclerosis Patients.Pharmacology research & perspectives · 2025Article
- Carnitine and Other Metabolites in Fibromyalgia a Clinical Perspective on a Mendelian Randomization Study.Journal of pain research · 2025Article
- The potential of repurposing clemastine to promote remyelination.Frontiers in cellular neuroscience · 2025Review
- Intrinsic retinoic acid synthesis is required for oligodendrocyte progenitor expansion during CNS remyelination.Frontiers in cellular neuroscience · 2025Article
- Hypertension may lead to cognitive dysfunction in older adults via methylmalonic acid: evidence from NHANES 2011-2014 population.BMC geriatrics · 2024Article
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- Neutral Red Labeling: A Novel Vital Staining Method for Investigating Central and Peripheral Nervous System Lesions.Acta histochemica et cytochemica · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Regulation of myeloid cell activity is critical for successful myelin regeneration (remyelination) in demyelinating diseases, such as multiple sclerosis (MS). Here, we show aromatic alpha-keto acids (AKAs) generated from the amino acid oxidase, interleukin-4 induced 1 (IL4I1), promote efficient remyelination in mouse models of MS. During remyelination, myeloid cells upregulated the expression of IL4I1. Conditionally knocking out IL4I1 in myeloid cells impaired remyelination efficiency. Mice lacking IL4I1 expression exhibited a reduction in the AKAs, phenylpyruvate, indole-3-pyruvate, and 4-hydroxyphenylpyruvate, in remyelinating lesions. Decreased AKA levels were also observed in people with MS, particularly in the progressive phase when remyelination is impaired. Oral administration of AKAs modulated myeloid cell-associated inflammation, promoted oligodendrocyte maturation, and enhanced remyelination in mice with focal demyelinated lesions. Transcriptomic analysis revealed AKA treatment induced a shift in metabolic pathways in myeloid cells and upregulated aryl hydrocarbon receptor activity in lesions. Our results suggest myeloid cell-associated aromatic amino acid metabolism via IL4I1 produces AKAs in demyelinated lesions to enable efficient remyelination. Increasing AKA levels or targeting related pathways may serve as a strategy to facilitate the regeneration of myelin in inflammatory demyelinating conditions.
Identifiers
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.