ArticleNeuromolecular medicine2025
Unraveling the Role of NeuroD2 in Ischemic Pathophysiology: Insight into Neuroprotection Mechanisms Associated with AKT Survival Kinase.
Article in Neuromolecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Multi-omics technologies: Novel tools and methods for assessing nerve injury and regeneration.Neural regeneration research · 2026Article
- Special Issue "Brain Injury: New Insights into Mechanisms and Future Promising Treatments".Biomedicines · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
NeuroD2 (ND2), a neuron-specific transcription factor, is essential in neural differentiation and neuroplasticity, yet its regulation under neuronal injury is barely uncovered. Effective treatment strategies for ischemic conditions require extensive knowledge of the signaling pathways and mechanisms underlying ischemic pathophysiology. This study aims to uncover the neuroprotective role of ND2 in ischemia and its interactions with critical signaling pathways implicated in recovery. An in vitro ischemic stroke model oxygen-glucose deprivation (OGD) method was applied to neuro-2A (N2a) cells with lentiviral ND2 (LvND2) overexpression. DNA fragmentation and cell survival assays indicated ND2's neuroprotective and anti-apoptotic effects under OGD conditions. Proteomic profiling and interaction analyses showed that LvND2 regulated the synthesis of cellular signaling, proliferation and cell adhesion-related proteins, such as MAPK3, Mki67, and NCAM. Additionally, a positive correlation was observed between ND2 expression and phosphorylated AKT levels. To investigate the interaction between ND2 and the PI3K/AKT signaling pathway, the pathway was pharmacologically inhibited with Wortmannin 30 min before OGD induction. After 8 h of OGD followed by 16 h of reperfusion, cell survival, DNA fragmentation, and Western blot analyses were performed. LvND2 administration alone increased cellular survival, whereas its combination with Wortmannin resulted in decreased cell survival. Additionally, LvND2 alone reduced the number of TUNEL-positive cells, while its combination with Wortmannin remains non-significant. These findings suggest that ND2 and AKT function in a coordinated manner within the PI3K/AKT survival pathway. ND2 may modulate AKT activity, highlighting its potential as a therapeutic target for addressing ischemic pathophysiology through molecular therapies.
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Registered trials
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