ArticleBiochemistry and biophysics reports2024
Unveiling functionality and conducting two-sample mendelian randomization on WGCNA-identified oxidative stress-related hub genes in metabolic dysfunction-associated fatty liver disease.
Article in Biochemistry and biophysics reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) shows accelerated development under the impact of oxidative stress (OS). There is an imperative to identify OS-related biomarkers in MAFLD and explore their potential mechanistic insights. The objective of this study was to identify OS-related biomarkers in MAFLD and explore their potential mechanisms. DEG analysis was performed using GSE17470 and GSE24807 datasets. An investigative exploration utilizing WGCNA was executed to elucidate hub OS-related genes. The intersection of OS-related hub genes identified by WGCNA and DEGs was systematically employed for thorough analyses. A mendelian randomization (MR) study examined the causal effect of C-reactive protein (CRP) on MAFLD. 59 OS-related DEGs were identified in MAFLD. WGCNA revealed 100 OS-related hub genes in MAFLD. Sixteen OS-related genes have been delineated as critical components in MAFLD. Enrichment analyses, employing GO and KEGG pathways, revealed pathways enriched with these genes. Following PPI analyses, the highest-ranking ten hub genes demonstrating abnormal expression were determined. Ultimately, a two-sample MR analysis demonstrated a causal link between the hub gene CRP and the occurrence of MAFLD. In this study, we harnessed WGCNA to formulate a co-expression network and identified hub OS-related DEGs in MAFLD. Additionally, the hub gene CRP exhibited a significant correlation with the predisposition to MAFLD. These findings offer innovative perspectives on the applications of OS-associated genes in individuals afflicted with MAFLD.
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