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Cited by 44Treatment of Major DepressionNeuroscience and Neuropharmacology ResearchStress Responses and Cortisol

The DOI matches its Crossref record; 89 of the 89 references it cites were found in a registry or an index.

PI3K/AKT/GSK3β/CRMP-2-mediated neuroplasticity in depression induced by stress

Wu, Zuotian, Wang, Gaohua, Wei, Yanyan, Xiao, Ling, Wang, Huiling·2018·Neuroreport
DOI 10.1097/wnr.0000000000001096
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Abstract

Early neurodevelopmental dysplasia or disorder is an important stimulus for depression, but early stress can easily damage nerve development and lead to decreased neural plasticity. Because of the characteristics of nerve cell, nerve loop, structure instability and so on, stress can often lead to the occurrence and recurrence of depression. Stress is often associated with the release of inflammatory factors in the central nervous system. Recent studies suggest that neuroinflammatory factors are most likely involved in the occurrence and development of stress-induced depression, attacking neuronal cells through central inflammatory factors. The changes in neural plasticity, such as microtubule system of nerve scaffold, extension of axonal dendrites, regeneration of nerve junctions, disturbance of neurotransmitter synthesis, transmission and release, and abnormal synapses, cause abnormal transmission of information between nerve cells and cause symptoms of depression. The changes in the structure of neural stent microtubules are closely related to the neuroplastic damage of depression induced by stress. Our previous studies and current studies have found that the AKT/GSK3β/CRMP-2 pathway mediates the changes in neural stent microtubule plasticity. There is an interaction between central inflammatory factors and this pathway. Therefore, from the point of view of neuritis injury and the plasticity change of nerve scaffold, it can be concluded that after the activation and release of central inflammatory factor under stress, the possible mechanism of depression is mediated by the AKT/GSK3β/CRMP-2 pathway by changing the normal structure and function of the central nervous cell scaffold microtubule system.

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Crossref · 10.1097/wnr.0000000000001096

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89 of 89 references verified0 citation errors · 0 not checkable

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Citations

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Show all 89 references

Research works printed but not linked: 5

  1. Li, 2017, Valproate attenuates endoplasmic reticulum stress-induced apoptosis in SH-SY5Y cells via the AKT/GSK3beta signaling pathway, Int J Mol Sci, 18, 2
  2. Li, 2017, SDF-1/CXCR4 axis induces human dental pulp stem cell migration through FAK/PI3K/Akt and GSK3β/β-catenin pathways, Sci Rep, 7, 40161, 10.1038/srep40161 · DOI
  3. Bai, 2017, Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine, Psychopharmacology (Berl, 234, 1, 10.1007/s00213-017-4547-3 · DOI
  4. Fang, 2015, Role of the Akt/GSK-3β/CRMP-2 pathway in axon degeneration of dopaminergic neurons resulting from MPP+ toxicity, Brain Res, 1602, 9, 10.1016/j.brainres.2014.08.030 · DOI
  5. Cai, 2014, BDNF attenuates IL-1β-induced F-actin remodeling by inhibiting NF-κB signaling in hippocampal neurons, Neuro Endocrinol Lett, 35, 13

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Metadata

Authors
Wu, Z., Wang, G., Wei, Y., Xiao, L., & Wang, H.
Affiliations
Renmin Hospital of Wuhan University (CN)
Corresponding author
  • Wu, Zuotian
  • Wang, Gaohua
  • Wang, Huiling
ORCID
Venue
Neuroreport
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2018-10-17
Volume
29
Issue
15
Pages
1256-1263
ISSN
0959-4965 (ISSN-L)
DOI
10.1097/wnr.0000000000001096
OpenAlex
W2887715260
Cited by
44
References
89
Citations by year
2025: 5 · 2024: 4 · 2023: 5 · 2022: 4 · 2021: 15 · 2020: 9 · 2019: 1 · 2018: 1
FWCI
4.19
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroreport (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
stress-induced depression, neuroplasticity, neuroinflammation, microtubule cytoskeleton, synaptic dysfunction, neurotransmission, early life stress
MeSH terms
Glycogen Synthase Kinase 3 beta, Animals, Depressive Disorder, Humans, Nerve Tissue Proteins, Neuronal Plasticity, Stress, Psychological, Phosphatidylinositol 3-Kinases, Intercellular Signaling Peptides and Proteins, Proto-Oncogene Proteins c-akt

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