ArticleJournal of translational medicine2023
Exploring the molecular mechanism of comorbidity of autism spectrum disorder and inflammatory bowel disease by combining multiple data sets.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting Osteoporosis-Osteoarthritis Comorbidity: Multi-Omics Identification of SON and Exploration of Therapeutic Agents.International journal of molecular sciences · 2026Article
- Remimazolam Ameliorates Autistic-Like Behaviors via Suppression of Ferroptosis in VTA Dopaminergic Neurons in a Mouse Model of ASD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Analysis of the Genetic Comorbid Mechanisms of Type 2 Diabetes, Alzheimer's Disease, and Hypertension Using Network Modularization.BioMed research international · 2026Article
- IL1B-centered immune dysregulation involving IL7R, CCR7, ITGB2 and IRF1 across insomnia and inflammatory bowel disease.Frontiers in immunology · 2026Article
- Gut microbiota-derived metabolites target C5AR1/KDM2A/HCAR3 axis in inflammatory bowel disease: a multi-machine learning algorithms and molecular docking study.Frontiers in cellular and infection microbiology · 2026Article
- Transcriptomic landscape of human circular RNAs: unveiling molecular mechanisms in high-altitude adaptation.Frontiers in genetics · 2026Article
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- Integrated bioinformatics analysis to develop diagnostic models for malignant transformation of chronic proliferative diseases.Blood science (Baltimore, Md.) · 2025Article
- Multi-omics insight into the molecular networks of mental disorder related genetic pathways in the pathogenesis of inflammatory bowel disease.Translational psychiatry · 2025Article
- Screening of biomarkers for diagnosing chronic kidney disease and heart failure with preserved ejection fraction through bioinformatics analysis.Biochemistry and biophysics reports · 2025Article
- Identification of the Shared Gene Signatures of HCK, NOG, RNF125 and Biological Mechanism in Pediatric Acute Lymphoblastic Leukaemia and Pediatric Sepsis.Molecular biotechnology · 2025Article
- Identification of hub modules and therapeutic targets associated with CD8Scientific reports · 2024Article
- Dietary intake and gastrointestinal symptoms are altered in children with Autism Spectrum Disorder: the relative contribution of autism-linked traits.Nutrition journal · 2024Article
- Identification of cuproptosis-related molecular classification and characteristic genes in ulcerative colitis.Heliyon · 2024Article
- Assessing the biobehavioral effects of ultramicronized-palmitoylethanolamide monotherapy in autistic adults with different severity levels: a report of two cases.Frontiers in psychiatry · 2024Article
- The shared circulating diagnostic biomarkers and molecular mechanisms of systemic lupus erythematosus and inflammatory bowel disease.Frontiers in immunology · 2024Article
- Analysis of complement system and its related factors in Alzheimer's disease.BMC neurology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutism spectrum disorder (ASD) is a neurodevelopmental disorder that is difficult to diagnose. Inflammatory bowel disease (IBD) is a common chronic digestive disease. Previous studies have shown a potential correlation between ASD and IBD, but the pathophysiological mechanism remains unclear. The purpose of this research was to examine the biological mechanisms underlying the differentially expressed genes (DEGs) of ASD and IBD using bioinformatics tools.
methodsLimma software was used to evaluate the DEGs between ASD and IBD. The GSE3365, GSE18123, and GSE150115 microarray data sets were acquired from the Gene Expression Omnibus (GEO) database. We then performed 6 analyses, namely, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional annotation; weighted gene coexpression network analysis; correlation analysis of hub genes with autophagy, ferroptosis and immunity; transcriptional regulation analysis of hub genes; single-cell sequencing analysis; and potential therapeutic drug prediction.
resultsA total of 505 DEGs associated with ASD and 616 DEGs associated with IBD were identified, and 7 genes overlapped between these sets. GO and KEGG analyses revealed several pathways enriched in both diseases. A total of 98 common genes related to ASD and IBD were identified by weighted gene coexpression network analysis (WGCNA), and 4 hub genes were obtained by intersection with the 7 intersecting DEGs, which were PDGFC, CA2, GUCY1B3 and SDPR. We also found that 4 hub genes in the two diseases were related to autophagy, ferroptosis or immune factors. In addition, motif-TF annotation analysis showed that cisbp__M0080 was the most relevant motif. We also used the Connectivity Map (CMap) database to identify 4 potential therapeutic agents.
conclusionThis research reveals the shared pathogenesis of ASD and IBD. In the future, these common hub genes may provide new targets for further mechanistic research as well as new therapies for patients with ASD and IBD.
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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.