ArticleNeuron2019
Glutathione S-Transferase Regulates Mitochondrial Populations in Axons through Increased Glutathione Oxidation.
Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 74 citations in OpenAlex.
- Glutathione in Our Diet and Its Role in the Body: From Disease Prevention to Anti-Aging.Nutrients · 2026Review
- Astrocytic GSTM2-STAT3 interaction ameliorates the diabetes associated cognitive dysfunction via targeting mitochondrial defects and oxidative stress.Redox biology · 2026Article
- Post-translational modifications in hepatocellular carcinoma: mechanisms and therapeutic potential.Medical oncology (Northwood, London, England) · 2025Review
- Metabolic coupling of ROS generation and antioxidant synthesis by the GABA shunt pathway in myeloid-like blood progenitor cells of Drosophila.PLoS genetics · 2025Article
- Mechanisms underlying targeted mitochondrial therapy for programmed cardiac cell death.Frontiers in physiology · 2025Review
- Adenosine diphosphate released from stressed cells triggers mitochondrial transfer to achieve tissue homeostasis.PLoS biology · 2024Article
- A neuron-glia lipid metabolic cycle couples daily sleep to mitochondrial homeostasis.Nature neuroscience · 2024Article
- N6-methyladenosine facilitates mitochondrial fusion of colorectal cancer cells via induction of GSH synthesis and stabilization of OPA1 mRNA.National science review · 2024Article
- Mitophagy in Alzheimer's Disease: A Bibliometric Analysis from 2007 to 2022.Journal of Alzheimer's disease reports · 2024Article
- Cdk12 maintains the integrity of adult axons by suppressing actin remodeling.Cell death discovery · 2023Article
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment.Antioxidants (Basel, Switzerland) · 2023Review
- mRNA Sequencing Reveals Upregulation of Glutathione S-Transferase Genes duringMicroorganisms · 2023Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Insights fromFrontiers in neuroscience · 2023Review
- S-Glutathionylation and S-Nitrosylation in Mitochondria: Focus on Homeostasis and Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Oral Administration of Glutathione Trisulfide Increases Reactive Sulfur Levels in Dorsal Root Ganglion and Ameliorates Paclitaxel-Induced Peripheral Neuropathy in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Recent insights into the role of glia and oxidative stress in Alzheimer's disease gained from Drosophila.Current opinion in neurobiology · 2022Review
- Glutathione S-transferases Control astrocyte activation and neuronal health during neuroinflammation.Frontiers in molecular biosciences · 2022Article
- Detailed Imaging of Mitochondrial Transport and Precise Manipulation of Mitochondrial Function with Genetically Encoded Photosensitizers in Adult Drosophila Neurons.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Mitochondria are essential in long axons to provide metabolic support and sustain neuron integrity. A healthy mitochondrial pool is maintained by biogenesis, transport, mitophagy, fission, and fusion, but how these events are regulated in axons is not well defined. Here, we show that the Drosophila glutathione S-transferase (GST) Gfzf prevents mitochondrial hyperfusion in axons. Gfzf loss altered redox balance between glutathione (GSH) and oxidized glutathione (GSSG) and initiated mitochondrial fusion through the coordinated action of Mfn and Opa1. Gfzf functioned epistatically with the thioredoxin peroxidase Jafrac1 and the thioredoxin reductase 1 TrxR-1 to regulate mitochondrial dynamics. Altering GSH:GSSG ratios in mouse primary neurons in vitro also induced hyperfusion. Mitochondrial changes caused deficits in trafficking, the metabolome, and neuronal physiology. Changes in GSH and oxidative state are associated with neurodegenerative diseases like Alzheimer's. Our demonstration that GSTs are key in vivo regulators of axonal mitochondrial length and number provides a potential mechanistic link.
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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.