ReviewFrontiers in neuroscience2025
Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.
Review in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Reprogramming the oxidative microenvironment: Antioxidant nanoplatforms for central nervous system repair.Materials today. Bio · 2026Review
- An Integrated Analysis of Manganese Metabolism-Related Genes and Their Association With Biomarkers, Immune Infiltration, and Clinical Subtypes in Alzheimer's Disease.Genes, brain, and behavior · 2026Article
- Cholinergic Phenotypes of Acetyl-CoA with ATP-Citrate Lyase Link.International journal of molecular sciences · 2026Review
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Authors and funding
6 authors.
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Abstract
Mitochondrial dysfunction is an important cause for neurodegeneration, often associated with dyshomeostasis of reactive oxygen species, i.e., oxidative stress. However, apart from ATP production, mitochondria have many other functions the aberration of which may impact neurons in very different ways. Oxidative stress can cause the deterioration of axonal microtubule bundles, thus critically affecting the highways for life-sustaining transport and providing a potential path to neurodegeneration. We recently found that aberrant transport of mitochondria can have this effect by causing oxidative stress. We therefore asked which aberrations of mitochondrial physiology might impact microtubules, which of these might explain the observed consequences of aberrant mitochondrial transport, and whether mitochondria-induced microtubule phenotypes are always mediated by oxidative stress. Using one consistent
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