ArticleMolecular neurobiology2019
Synergy in Disruption of Mitochondrial Dynamics by Aβ (1-42) and Glia Maturation Factor (GMF) in SH-SY5Y Cells Is Mediated Through Alterations in Fission and Fusion Proteins.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- Rethinking on bile acid-brain axis: decoding neurotoxic and neuroprotective landscape in aging and Alzheimer's disease.Biogerontology · 2026Review
- Crosstalk between mitochondrial dysfunction and benign prostatic hyperplasia: unraveling the intrinsic mechanisms.The Canadian journal of urology · 2025Review
- Mitochondrial quality control disorder in neurodegenerative disorders: Potential and advantages of traditional Chinese medicines.Journal of pharmaceutical analysis · 2025Review
- Nuclear respiratory factor-1 (NRF1) induction drives mitochondrial biogenesis and attenuates amyloid beta-induced mitochondrial dysfunction and neurotoxicity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Deletion of MAPL ameliorates septic cardiomyopathy by mitigating mitochondrial dysfunction.Journal of translational medicine · 2024Article
- Lactate Protects Microglia and Neurons from Oxygen-Glucose Deprivation/Reoxygenation.Neurochemical research · 2024Article
- Parkinson's Disease Dementia Patients: Expression of Glia Maturation Factor in the Brain.International journal of molecular sciences · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- Cellulose ether treatment inhibits amyloid beta aggregation, neuroinflammation and cognitive deficits in transgenic mouse model of Alzheimer's disease.Journal of neuroinflammation · 2023Article
- Mitophagy regulation in aging and neurodegenerative disease.Biophysical reviews · 2023Review
- SIRT7 Deficiency Protects against AβInternational journal of molecular sciences · 2022Article
- Amyloid-β impairs mitochondrial dynamics and autophagy in Alzheimer's disease experimental models.Scientific reports · 2022Article
- Inhibition of calpain reduces cell apoptosis by suppressing mitochondrial fission in acute viral myocarditis.Cell biology and toxicology · 2022Article
- Mitochondrial dynamics and biogenesis indicators may serve as potential biomarkers for diagnosis of myasthenia gravis.Experimental and therapeutic medicine · 2022Article
- Acute Traumatic Brain Injury-Induced Neuroinflammatory Response and Neurovascular Disorders in the Brain.Neurotoxicity research · 2021Article
- Neuroinflammation Mediated by Glia Maturation Factor Exacerbates Neuronal Injury in anJournal of neurotrauma · 2020Article
- Absence of Glia Maturation Factor Protects from Axonal Injury and Motor Behavioral Impairments after Traumatic Brain Injury.Experimental neurobiology · 2020Article
- Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury.Mediators of inflammation · 2020Article
- Glia Maturation Factor in the Pathogenesis of Alzheimer's disease.Open access journal of neurology & neurosurgery · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
The pathological form of amyloid beta (Aβ) peptide is shown to be toxic to the mitochondria and implicates this organelle in the progression and pathogenesis of Alzheimer's disease (AD). Mitochondria are dynamic structures constantly undergoing fission and fusion, and altering their shape and size while traveling through neurons. Mitochondrial fission (Drp1, Fis1) and fusion (OPA1, Mfn1, and Mfn2) proteins are balanced in healthy neuronal cells. Glia maturation factor (GMF), a neuroinflammatory protein isolated and cloned in our laboratory plays an important role in the pathogenesis of AD. We hypothesized that GMF, a brain-localized inflammatory protein, promotes oxidative stress-mediated disruption of mitochondrial dynamics by alterations in mitochondrial fission and fusion proteins which eventually leads to apoptosis in the Aβ (1-42)-treated human neuroblastoma (SH-SY5Y) cells. The SH-SY5Y cells were incubated with GMF and Aβ (1-42) peptide, and mitochondrial fission and fusion proteins were analyzed by immunofluorescence, western blotting, and co-immunoprecipitation. We report that SH-SY5Y cells incubated with GMF and Aβ (1-42) promote mitochondrial fragmentation, by potentiating oxidative stress, mitophagy and shifts in the Bax/Bcl2 expression and release of cytochrome-c, and eventual apoptosis. In the present study, we show that GMF and Aβ treatments significantly upregulate fission proteins and downregulate fusion proteins. The study shows that extracellular GMF is an important inflammatory mediator that mediates mitochondrial dynamics by altering the balance in fission and fusion proteins and amplifies similar effects promoted by Aβ. Upregulated GMF in the presence of Aβ could be an additional risk factor for AD, and their synergistic actions need to be explored as a potential therapeutic target to suppress the progression of AD.
Indexed as
Identifiers
What OpenQuestion holds
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.