{"title":"Identification of mitophagy and ferroptosis-related hub genes associated with intracerebral haemorrhage through bioinformatics analysis.","authors":"Yan Wang, Rufeng Wang, Jianzhong Zhu, Ling Chen","doi":"10.1080/03014460.2024.2334719","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Mitophagy and ferroptosis occur in intracerebral haemorrhage (ICH) but our understanding of mitophagy and ferroptosis-related genes remains incomplete.</p><p><strong>Aim: </strong>This study aims to identify shared ICH genes for both processes.</p><p><strong>Methods: </strong>ICH differentially expressed mitophagy and ferroptosis-related genes (DEMFRGs) were sourced from the GEO database and literature. Enrichment analysis elucidated functions. Hub genes were selected via STRING, MCODE, and MCC algorithms in Cytoscape. miRNAs targeting hubs were predicted using miRWalk 3.0, forming a miRNA-hub gene network. Immune microenvironment variances were assessed with MCP and TIMER. Potential small molecules for ICH were forecasted <i>via</i> CMap database.</p><p><strong>Results: </strong>64 DEMFRGs and ten hub genes potentially involved in various processes like ferroptosis, TNF signalling pathway, MAPK signalling pathway, and NF-kappa B signalling pathway were discovered. Several miRNAs were identified as shared targets of hub genes. The ICH group showed increased infiltration of monocytic lineage and myeloid dendritic cells compared to the Healthy group. Ten potential small molecule drugs (e.g. Zebularine, TWS-119, CG-930) were predicted <i>via</i> CMap.</p><p><strong>Conclusion: </strong>Several shared genes between mitophagy and ferroptosis potentially drive ICH progression <i>via</i> TNF, MAPK, and NF-kappa B pathways. These results offer valuable insights for further exploring the connection between mitophagy, ferroptosis, and ICH.</p>","PeriodicalId":50765,"journal":{"name":"Annals of Human Biology","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Human Biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/03014460.2024.2334719","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/12 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ANTHROPOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Mitophagy and ferroptosis occur in intracerebral haemorrhage (ICH) but our understanding of mitophagy and ferroptosis-related genes remains incomplete.
Aim: This study aims to identify shared ICH genes for both processes.
Methods: ICH differentially expressed mitophagy and ferroptosis-related genes (DEMFRGs) were sourced from the GEO database and literature. Enrichment analysis elucidated functions. Hub genes were selected via STRING, MCODE, and MCC algorithms in Cytoscape. miRNAs targeting hubs were predicted using miRWalk 3.0, forming a miRNA-hub gene network. Immune microenvironment variances were assessed with MCP and TIMER. Potential small molecules for ICH were forecasted via CMap database.
Results: 64 DEMFRGs and ten hub genes potentially involved in various processes like ferroptosis, TNF signalling pathway, MAPK signalling pathway, and NF-kappa B signalling pathway were discovered. Several miRNAs were identified as shared targets of hub genes. The ICH group showed increased infiltration of monocytic lineage and myeloid dendritic cells compared to the Healthy group. Ten potential small molecule drugs (e.g. Zebularine, TWS-119, CG-930) were predicted via CMap.
Conclusion: Several shared genes between mitophagy and ferroptosis potentially drive ICH progression via TNF, MAPK, and NF-kappa B pathways. These results offer valuable insights for further exploring the connection between mitophagy, ferroptosis, and ICH.
期刊介绍:
Annals of Human Biology is an international, peer-reviewed journal published six times a year in electronic format. The journal reports investigations on the nature, development and causes of human variation, embracing the disciplines of human growth and development, human genetics, physical and biological anthropology, demography, environmental physiology, ecology, epidemiology and global health and ageing research.