ArticleNature aging2025
Transcriptional profiles of mouse oligodendrocyte precursor cells across the lifespan.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Rethinking the Oligodendrocyte Progenitor Cell: One Cell, Many Functions.The European journal of neuroscience · 2026Review
- Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease.Neuroscience bulletin · 2026Review
- Temporal changes in metabolism guide oligodendrocyte precursor cell dynamics in aging and multiple sclerosis.Neuron · 2026Article
- From insights to innovations: evaluating preclinical paradigms in demyelinating disease therapeutics.Lab animal · 2026Review
- Hypoxia-induced autophagic degradation of HIF-1α attenuates cellular aging and extends mammalian lifespan.Nature aging · 2026Article
- Metabolic Symbiosis and Vulnerability in the CNS Axon-Myelin Unit.Cellular and molecular neurobiology · 2026Review
- Article
- Oligodendrocyte: Development, Plasticity, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Myelin is repaired by constitutive differentiation of oligodendrocyte progenitors.Science (New York, N.Y.) · 2026Article
- Oligodendrocyte precursor cell AMPA receptors differ with age and brain region while kainate receptors remain stable.iScience · 2025Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Oligodendrocyte progenitor cell responses to inflammatory demyelination with aging.Research square · 2025Article
- Review
- Dynamic Intercellular Networks in the CNS: Mechanisms of Crosstalk from Homeostasis to Neurodegeneration.International journal of molecular sciences · 2025Review
- Glial Cells and Aging: From the CNS to the Cerebellum.International journal of molecular sciences · 2025Review
- Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities.Molecular neurodegeneration · 2025Review
- The Power of Neuroglia in Driving Brain Function.Neurochemical research · 2025Review
- MHC class I and II expression and induction in oligodendrocytes varies with age.Scientific reports · 2025Article
- To recruit or to graft? Comparing the recruitment of resident non-neuronal cells by lineage reprogramming with engraftment of stem cell-derived neurons for neuronal replacement therapies.Frontiers in neuroscience · 2025Review
Corrections and comments
- Update of
Authors and funding
10 authors.
Funding
Abstract
Oligodendrocyte progenitor cells (OPCs) are highly dynamic, widely distributed glial cells of the central nervous system responsible for generating myelinating oligodendrocytes throughout life. However, the rates of OPC proliferation and differentiation decline dramatically with aging, which may impair homeostasis, remyelination and adaptive myelination during learning. To determine how aging influences OPCs, we generated a transgenic mouse line (Matn4-mEGFP) and performed single-cell RNA sequencing, providing enhanced resolution of transcriptional changes during key transitions from quiescence to proliferation and differentiation across the lifespan. We found that aging induces distinct transcriptomic changes in OPCs in different states, including enhanced activation of HIF-1α and WNT pathways. Pharmacological inhibition of these pathways in aged OPCs was sufficient to increase their ability to differentiate in vitro. Ultimately, Matn4-mEGFP mouse line and the sequencing dataset of cortical OPCs across ages will help to define the molecular changes guiding OPC behavior in various physiological and pathological contexts.
Indexed as
Identifiers
40164771What Socratic 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 Socratic graph.