ArticleCell death and differentiation2014
Tumor necrosis factor-α impairs oligodendroglial differentiation through a mitochondria-dependent process.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
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Who cites it
99 citing papers in PubMed, 143 citations in OpenAlex.
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- The shifting landscape of the preterm brain.Neuron · 2025Review
- Mitochondrial genome analysis of the endangered Oreocharis esquirolii: insights into evolutionary adaptation and conservation.BMC plant biology · 2025Article
- The Effect of Tumor Necrosis Factor-α and Interleu-Kin-1β on the Restorative Properties of Human Oligodendrocyte Precursor Cells In Vitro.Bioengineering (Basel, Switzerland) · 2025Article
- Assembly and analysis of the complete mitochondrial genome of Leonurus japonicus (Lamiaceae).Scientific reports · 2025Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial defects, affecting parameters such as mitochondrial number and shape, levels of respiratory chain complex components and markers of oxidative stress, have been associated with the appearance and progression of multiple sclerosis. Nevertheless, mitochondrial physiology has never been monitored during oligodendrocyte progenitor cell (OPC) differentiation, especially in OPCs challenged with proinflammatory cytokines. Here, we show that tumor necrosis factor alpha (TNF-α) inhibits OPC differentiation, accompanied by altered mitochondrial calcium uptake, mitochondrial membrane potential, and respiratory complex I activity as well as increased reactive oxygen species production. Treatment with a mitochondrial uncoupler (FCCP) to mimic mitochondrial impairment also causes cells to accumulate at the progenitor stage. Interestingly, AMP-activated protein kinase (AMPK) levels increase during TNF-α exposure and inhibit OPC differentiation. Overall, our data indicate that TNF-α induces metabolic changes, driven by mitochondrial impairment and AMPK activation, leading to the inhibition of OPC differentiation.
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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.