ArticleFrontiers in psychiatry2022
Comprehensive analysis of endoplasmic reticulum stress and immune infiltration in major depressive disorder.
Article in Frontiers in psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Continuous Alterations in the Gut Microbial Landscape Associated With Suicidal Ideation in First-Episode Drug-naïve Major Depressive Disorder.CNS neuroscience & therapeutics · 2026Article
- Review
- Mendelian randomization and transcriptome analysis reveal depression-driven regulatory patterns of the immune microenvironment in myocardial infarction and heart failure.Frontiers in immunology · 2026Article
- The identification and validation of histone acetylation-related biomarkers in depression disorder based on bioinformatics and machine learning approaches.Frontiers in neuroscience · 2025Article
- Quantitative proteomics combined independent PRM analysis reveals the mitochondrial and synaptic mechanism underlying norisoboldine's antidepressant effects.Translational psychiatry · 2024Article
- A characteristic cerebellar biosignature for bipolar disorder, identified with fully automatic machine learning.IBRO neuroscience reports · 2023Article
- Cuproptosis-related genes prediction feature and immune microenvironment in major depressive disorder.Heliyon · 2023Article
- Identification of a diagnostic model and molecular subtypes of major depressive disorder based on endoplasmic reticulum stress-related genes.Frontiers in psychiatry · 2023Article
- Identification of Ferroptosis-Related Hub Genes as Diagnosis Biomarkers and Therapeutic Monitoring for Major Depressive Disorder Diagnosis.IET systems biologyArticle
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Major depressive disorder (MDD) is a life-threatening, debilitating mental health condition. An important factor in the development of depression is endoplasmic reticulum stress (ERS). However, their roles in MDD have not yet been established. The goal of this study was to examine ERS and its underlying molecular mechanisms in MDD. Methods: We used data from two microarray datasets (GSE98793 and GSE39653) and the GeneCards database to examine the reticulum stress-related differentially expressed genes (ERSR-DEGs) associated with MDD. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and Gene Set Variation Analysis (GSVA) were used to further investigate the function and mechanism of ERS in MDD. Moreover, we constructed protein-protein interaction (PPI) networks to identify hub genes as well as the regulatory network of microRNAs (miRNAs), transcription factors (TFs), and potential drugs related to ERSR-DEGs. CIBERSORT was then used to evaluate the immune activity of MDD samples and conduct a correlation analysis between the hub genes and immune cells. Results: In total, 37 ERSR-DEGs and five hub genes were identified (NCF1, MAPK14, CASP1, CYBA, and TNF). Functional enrichment analysis revealed that ERSR-DEGs were predominantly enriched in inflammation-and immunity-related pathways, such as tumor necrosis factor signaling, NF-κB signaling, and Toll-like receptor signaling pathways. Additionally, 179 miRNAs, 25 TFs, and 15 potential drugs were tested for their interactions with the ERSR-DEGs. CIBERSORT found high proportions of Tregs, monocytes, and macrophages M0 in the MDD samples. Among these, hub genes showed a significant correlation with immune cell infiltration in patients with MDD. Conclusions: NCF1, MAPK14, CASP1, CYBA, and TNF are potential ERS-related biomarkers for the diagnosis of MDD. Our research has revealed a significant correlation between immune cells and ERS-related genes with MDD. Not only did our study contribute to a better understanding of the regulatory mechanisms of ERS in underlying MDD pathology, but it also established a paradigm for future studies on ERS.
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