ArticleMolecular neurodegeneration2023
NF-κB is a critical mediator of post-mitotic senescence in oligodendrocytes and subsequent white matter loss.
Article in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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43 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Differential effects of environmental enrichment and physical exercise on glial biology in aging and aging-related conditions: a systematic review.Frontiers in cellular neuroscience · 2026Pooled it
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- Oligodendroglial Mutant Huntingtin Contributes to Neuroinflammation in Huntington's Disease Mice.Neuroscience bulletin · 2026Article
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- Transcriptional Heterogeneity of Oligodendrocytes: Molecular Basis of Diversity Across Development, Brain Regions, and Neurological Diseases.Neurology international · 2026Review
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- NF-κB activation in astrocytes impairs wound healing after traumatic brain injury in male mice.Nature communications · 2026Article
- Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex.Cell genomics · 2026Article
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy.Molecular psychiatry · 2026Article
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
- cGAS-STING signaling in brain aging and neurodegeneration: molecular links and therapeutic perspectives.Journal of neuroinflammation · 2025Review
- Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Aging-associated Increase of GATA4 levels in Articular Cartilage is Linked to Impaired Regenerative Capacity of Chondrocytes and Osteoarthritis.bioRxiv : the preprint server for biology · 2025Article
- Hyperoside inhibits PRRSV proliferation via the TLR4/NF-κB and p62-Nrf2-Keap1 signaling pathways, mediating inflammation and autophagy.Microbiology spectrum · 2025Article
- Identification of markers for neurescence through transcriptomic profiling of postmortem human brains.npj aging · 2025Article
- Functional Features of Senescent Cells and Implications for Therapy.International journal of molecular sciences · 2025Review
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Authors and funding
23 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammaging represents an accepted concept where the immune system shifts to a low-grade chronic pro-inflammatory state without overt infection upon aging. In the CNS, inflammaging is mainly driven by glia cells and associated with neurodegenerative processes. White matter degeneration (WMD), a well-known process in the aging brain, manifests in myelin loss finally resulting in motor, sensory and cognitive impairments. Oligodendrocytes (OL) are responsible for homeostasis and maintenance of the myelin sheaths, which is a complex and highly energy demanding process sensitizing these cells to metabolic, oxidative and other forms of stress. Yet, the immediate impact of chronic inflammatory stress like inflammaging on OL homeostasis, myelin maintenance and WMD remains open.
methodsTo functionally analyze the role of IKK/NF-κB signaling in the regulation of myelin homeostasis and maintenance in the adult CNS, we established a conditional mouse model allowing NF-κB activation in mature myelinating oligodendrocytes. IKK2-CA
resultsChronic NF-κB activation in mature OLs leads to aggravated neuroinflammatory conditions phenocopying brain inflammaging. As a consequence, IKK2-CA
conclusionsOur findings demonstrate an essential role of IKK/NF-κB signaling in mature, post-mitotic OLs in regulating stress-induced senescence in these cells. Moreover, our study identifies PoMICS as an important driving force of age-dependent WMD as well as of traumatic brain injury induced myelin defects.
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