ArticleBrain and behavior2025
Identification of Critical Signature in Post-Traumatic Stress Disorder Using Bioinformatics Analysis and in Vitro Analyses.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Ginsenoside Rh1 inhibits tumor growth in mice with colorectal cancer and depressive symptoms via modulation of the gut microbiota and tumor microenvironment.Molecular medicine reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundPost-traumatic stress disorder (PTSD) is a complex psychiatric condition that emerges following exposure to trauma and significantly affects daily functioning. Current research is focused on identifying effective treatments for PTSD. Advances in bioinformatics provide opportunities to elucidate the underlying mechanisms of PTSD.
methodsRNA sequencing (RNA-seq) datasets were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using GEO2R. Weighted gene co-expression network analysis (WGCNA) was employed to examine gene correlation patterns. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed for functional annotation and enrichment analysis, respectively. The MCODE plugin in Cytoscape software was utilized to analyze the protein-protein interaction (PPI) network. Anxiety and depression in a mice stress model were assessed using the open-field test (OFT), elevated plus maze test (EPMT), and forced swimming test (FST). Real-time quantitative PCR (qRT-PCR) was conducted to validate key genes in stress-exposed models.
resultsA total of 157 common upregulated DEGs and 53 common downregulated DEGs were identified in the amygdala (AMY) and the hippocampus (HIP). Notably enriched pathways included neuroactive ligand-receptor interaction, mechanistic target of rapamycin (mTOR) signaling pathway, nicotine addiction, and dopaminergic synapse. The PPI network identified four hub genes, with key pathways associated with nicotine addiction and dopaminergic synapse. qRT-PCR validation confirmed that the expression trends of these four genes were consistent with microarray data. Behavioral tests (OFT, EMPT, and FST) revealed significant changes.
conclusionThis study utilized bioinformatics and in vitro experiments to identify genes and pathways potentially crucial for PTSD development. Key genes were validated in a mouse model, providing insights into potential target genes for PTSD treatment.
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.