ArticleCommunications biology2021
Age-related injury responses of human oligodendrocytes to metabolic insults: link to BCL-2 and autophagy pathways.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Energy for myelination: Implications for metabolic disturbances in multiple sclerosis pathology.Neural regeneration research · 2026Article
- Age and Maturation Stage Linked Consequences of Fibrinogen on Human Oligodendroglia.Journal of neuroscience research · 2026Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- The role of Bcl‑2 in controlling the transition between autophagy and apoptosis (Review).Molecular medicine reports · 2025Review
- Pro-Inflammatory Molecules Implicated in Multiple Sclerosis Divert the Development of Human Oligodendrocyte Lineage Cells.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- From BBB to PPP: Bioenergetic requirements and challenges for oligodendrocytes in health and disease.Journal of neurochemistry · 2025Review
- The immunological role of oligodendrocytes: beyond myelin maintenance.Discovery immunology · 2025Review
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- Regulation of stress granule formation in human oligodendrocytes.Nature communications · 2024Article
- Review
- ALCAM on human oligodendrocytes mediates CD4 T cell adhesion.Brain : a journal of neurology · 2024Article
- The role of glial autophagy in Alzheimer's disease.Molecular psychiatry · 2023Review
- Pearls and Pitfalls of Isolating Rat OPCs for In Vitro Culture with Different Methods.Cellular and molecular neurobiology · 2023Article
- Mechanisms of metabolic stress induced cell death of human oligodendrocytes: relevance for progressive multiple sclerosis.Acta neuropathologica communications · 2023Article
- Emerging mitochondrial-mediated mechanisms involved in oligodendrocyte development.Journal of neuroscience research · 2023Review
- Transcriptional and bioinformatic analysis of GABAFrontiers in molecular neuroscience · 2023Article
- Neuronal ambient RNA contamination causes misinterpreted and masked cell types in brain single-nuclei datasets.Neuron · 2022Article
- Chronic oligodendrocyte injury in central nervous system pathologies.Communications biology · 2022Review
- Article
- Oligodendroglial Energy Metabolism and (re)Myelination.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin destruction and oligodendrocyte (OL) death consequent to metabolic stress is a feature of CNS disorders across the age spectrum. Using cells derived from surgically resected tissue, we demonstrate that young (<age 5) pediatric-aged sample OLs are more resistant to in-vitro metabolic injury than fetal O4+ progenitor cells, but more susceptible to cell death and apoptosis than adult-derived OLs. Pediatric but not adult OLs show measurable levels of TUNEL+ cells, a feature of the fetal cell response. The ratio of anti- vs pro-apoptotic BCL-2 family genes are increased in adult vs pediatric (<age 5) mature OLs and in more mature OL lineage cells. Lysosomal gene expression was increased in adult and pediatric compared to fetal OL lineage cells. Cell death of OLs was increased by inhibiting pro-apoptotic BCL-2 gene and autophagy activity. These distinct age-related injury responses should be considered in designing therapies aimed at reducing myelin injury.
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Registered trials
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