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New Insights into the Role of Inflammatory Pathways and Immune Cell Infiltration in Sleep Deprivation-Induced Atrial Fibrillation: An Integrated Bioinformatics and Experimental Study

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Název: New Insights into the Role of Inflammatory Pathways and Immune Cell Infiltration in Sleep Deprivation-Induced Atrial Fibrillation: An Integrated Bioinformatics and Experimental Study
Autoři: Junqing Liang, Baopeng Tang, Jun Shen, Manzeremu Rejiepu, Yankai Guo, Xiaoyan Wang, Shijie Shao, Fei Guo, Qin Wang, Ling Zhang
Zdroj: J Inflamm Res
Journal of Inflammation Research, Vol Volume 18, Pp 791-812 (2025)
Informace o vydavateli: Informa UK Limited, 2025.
Rok vydání: 2025
Témata: ybx1, inflammation, Pathology, RB1-214, atrial fibrillation, Therapeutics. Pharmacology, RM1-950, sleep deprivation, bioinformatic analysis, Original Research
Popis: BACKGROUND: The common occurrence of atrial fibrillation (AF) as a cardiac arrhythmia, along with its link to sleep deprivation (SD), is gaining more acknowledgment. Even with progress in comprehending the development of AF, the molecular connections between SD and AF are still not well-defined. The objective of this research was to pinpoint the shared molecular routes responsible for SD-induced AF and investigate possible treatment targets. METHODS: Utilizing bioinformatics, we examined two transcriptome datasets from the Gene Expression Omnibus (GEO) database to pinpoint genes with differential expression (DEGs) common to SD and AF. Analyses focusing on functional enrichment, such as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), were conducted to pinpoint crucial biological mechanisms and pathways. Furthermore, we utilized immunofluorescence and Western blot techniques to evaluate YBX1 expression and its role in activating NLRP3 inflammasomes in a rat model induced by SD. RESULTS: A total of 540 common DEGs were precisely identified between the AF and SD data collections. Studies emphasizing functional enrichment have highlighted the significance of inflammation pathways, particularly the NOD-like receptor signaling route. The application of machine learning uncovered four crucial genes—CDC5L, MAPK14, RAB5A, and YBX1—with YBX1 becoming the predominant gene in diagnostic processes. Investigating immune penetration revealed significant connections between YBX1 expression and specific immune cell types, notably CD8+ T cells and M1 macrophages. Live studies have demonstrated that SD amplifies the atrial electrical rearrangement, structural changes, the infiltration of inflammatory cells, and the heightened presence of YBX1 along with inflammasome elements. CONCLUSION: The research pinpoints YBX1 as a crucial gene in SD-related AF, possibly influencing its impact via the NOD-like receptor signaling route and the invasion of immune cells. The results offer crucial understanding of the molecular processes behind AF and propose YBX1 as a possible treatment focus to reduce the risk of AF caused by SD.
Druh dokumentu: Article
Other literature type
Jazyk: English
ISSN: 1178-7031
DOI: 10.2147/jir.s495777
Přístupová URL adresa: https://doaj.org/article/60a732cc165f4f4aa0751840ba600e2f
Rights: CC BY NC
URL: http://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at http://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (http://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (http://www.dovepress.com/terms.php).
Přístupové číslo: edsair.doi.dedup.....1a7b961e854c8976095daf660f73de26
Databáze: OpenAIRE
Popis
Abstrakt:BACKGROUND: The common occurrence of atrial fibrillation (AF) as a cardiac arrhythmia, along with its link to sleep deprivation (SD), is gaining more acknowledgment. Even with progress in comprehending the development of AF, the molecular connections between SD and AF are still not well-defined. The objective of this research was to pinpoint the shared molecular routes responsible for SD-induced AF and investigate possible treatment targets. METHODS: Utilizing bioinformatics, we examined two transcriptome datasets from the Gene Expression Omnibus (GEO) database to pinpoint genes with differential expression (DEGs) common to SD and AF. Analyses focusing on functional enrichment, such as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), were conducted to pinpoint crucial biological mechanisms and pathways. Furthermore, we utilized immunofluorescence and Western blot techniques to evaluate YBX1 expression and its role in activating NLRP3 inflammasomes in a rat model induced by SD. RESULTS: A total of 540 common DEGs were precisely identified between the AF and SD data collections. Studies emphasizing functional enrichment have highlighted the significance of inflammation pathways, particularly the NOD-like receptor signaling route. The application of machine learning uncovered four crucial genes—CDC5L, MAPK14, RAB5A, and YBX1—with YBX1 becoming the predominant gene in diagnostic processes. Investigating immune penetration revealed significant connections between YBX1 expression and specific immune cell types, notably CD8+ T cells and M1 macrophages. Live studies have demonstrated that SD amplifies the atrial electrical rearrangement, structural changes, the infiltration of inflammatory cells, and the heightened presence of YBX1 along with inflammasome elements. CONCLUSION: The research pinpoints YBX1 as a crucial gene in SD-related AF, possibly influencing its impact via the NOD-like receptor signaling route and the invasion of immune cells. The results offer crucial understanding of the molecular processes behind AF and propose YBX1 as a possible treatment focus to reduce the risk of AF caused by SD.
ISSN:11787031
DOI:10.2147/jir.s495777