ArticleNature communications2025
Senescent-like microglia limit remyelination through the senescence associated secretory phenotype.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed.
- Review
- Lithium as a Potential Senostatic Agent in Central Nervous System Aging and Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mitochondrial stress response drives microglial senescence.Nature neuroscience · 2026Article
- Single-cell multiomics connects 3D genome and transcriptome alterations in Alzheimer's disease.Science (New York, N.Y.) · 2026Article
- DNA Sensing and Neuroinflammation: Mechanistic Insights into cGAS-STING Biology and Therapeutic Translation in Age-Related Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Acid ceramidase modulates the lipid profile and exacerbates sensitivity to ferroptosis in WI-38 replicative senescent cells.Cell death & disease · 2026Article
- Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents: a pharmacological strategy to mitigate brain aging and cognitive decline.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Foamy microglia link oxylipins to disease progression in multiple sclerosis.Nature neuroscience · 2026Article
- Spatial mapping and senolytic targeting of senescent and disease-associated microglia in aged mouse brain white matter.Nature aging · 2026Article
- Coordinated transcriptional shifts in microglia and oligodendrocytes from neurodevelopment to inflammaging.npj aging · 2026Article
- Myelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside.Medicina (Kaunas, Lithuania) · 2026Review
- Integration Analysis of Bayesian and Machine Learning for Heterogeneity, Biomarkers, and Optimal Combination Regimens of Pucotenlimab in Solid Tumors.Cancer medicine · 2026Article
- Fluorescence-Guided Spatial Mapping of p21-Expressing Senescent Cells in Aged Liver at Single-Cell Resolution.Biomolecules · 2026Article
- Molecular and histological characterizations reveal two distinct senescent microglia populations in Niemann-Pick disease type C mouse model.GeroScience · 2026Article
- Review
- The Roles of Macrophage Lineage Cells (MLCs) in Brain Aging.CNS neuroscience & therapeutics · 2026Review
- Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities.Biomedicines · 2026Review
- Engineering Immune Cell to Counteract Aging and Aging-Associated Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- Neurovascular unit remodeling: focusing on glial cells in stroke injury and recovery.Frontiers in cellular neuroscience · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The capacity to regenerate myelin in the central nervous system diminishes with age. This decline is particularly evident in multiple sclerosis (MS), a chronic demyelinating disease. Whether cellular senescence, a hallmark of aging, contributes to remyelination impairment remains unknown. Here, we show that senescent cells accumulate within demyelinated lesions after injury, and treatments with senolytics enhances remyelination in young and middle-aged mice but not aged mice. In young mice, we observe the upregulation of senescence-associated transcripts, primarily in microglia and macrophages, after demyelination, followed by a reduction during remyelination. However, in aged mice, senescence-associated factors persist within lesions, correlating with inefficient remyelination. Proteomic analysis of the senescence-associated secretory phenotype (SASP) reveals elevated levels of CCL11/Eotaxin-1 in lesions of aged mice, which is found to inhibit oligodendrocyte maturation. These results suggest therapeutic targeting of SASP components, such as CCL11, may improve remyelination in aging and MS.
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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.