ArticleMedical molecular morphology2019
Interactions between mitochondria and endoplasmic reticulum in demyelinated axons.
Article in Medical molecular morphology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- From Obesity to Mitochondrial Dysfunction in Peripheral Tissues and in the Central Nervous System.Biomolecules · 2025Review
- The Emerging Role of Microglial Hv1 as a Target for Immunomodulation in Myelin Repair.Aging and disease · 2024Review
- Fatty Acids Play a Critical Role in Mitochondrial Oxidative Phosphorylation in Effector T Cells in Graft-versus-Host Disease.ImmunoHorizons · 2024Article
- The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.Frontiers in neuroscience · 2023Review
- Budding pouches and associated bubbles: 3D visualization of exo-membrane structures inFrontiers in cellular and infection microbiology · 2022Article
- Paranodal Axoglial Junctions, an Essential Component in Axonal Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Demyelination of the Optic Nerve: An Underlying Factor in Glaucoma?Frontiers in aging neuroscience · 2021Review
- Sodium-glucose co-transporter (SGLT) inhibitor restores lost axonal varicosities of the myenteric plexus in a mouse model of high-fat diet-induced obesity.Scientific reports · 2020Article
- Methodological Improvements With Conductive Materials for Volume Imaging of Neural Circuits by Electron Microscopy.Frontiers in neural circuits · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Demyelination leads to axonal changes that involve the functions and dynamics of axonal mitochondria supporting metabolism and survival of axons. However, the changes in the physical interactions between mitochondria and endoplasmic reticulum, called mitochondria-associated membranes, are poorly understood in demyelinated axons. In this study, we investigated the three-dimensional ultrastructural changes in membrane juxtapositions between mitochondria and endoplasmic reticulum in axons of a chronic progressive demyelination mouse model caused by extra copies of proteolipid protein (PLP4e). In the optic nerve of PLP4e mice, most axons were ensheathed by myelin by age 1 month, but were demyelinated by age 5 months. At age 1 month, mitochondria in PLP4e mice were slightly larger than those in wild-type mice, while the size and frequency of juxtaposition were similar. At age 5 months, the sizes of mitochondria and size of juxtaposition in PLP4e mice were prominently larger than those in wild-type mice. In degenerating axons under demyelination, the enlargement of mitochondria was diminished, while the density and frequency of juxtaposition were similar to those of non-degenerating axons. These results suggest that interactions between mitochondria and ER are enhanced in chronically demyelinated axons and maintained during axonal degeneration in hereditary myelin diseases.
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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.