MUC1 and CREB3 are Hub Ferroptosis Suppressors for Nucleus Pulposus and Annulus Fibrosus Degeneration by Integrated Bioinformatics and Experimental Verification

Journal of Inflammation Research, Год журнала: 2024, Номер Volume 17, С. 8965 - 8984

Опубликована: Ноя. 1, 2024

Ferroptosis is an underlying mechanism for various degenerative diseases, but its role in intervertebral disc degeneration remains elusive. This study aims to explore the key ferroptosis-related genes and nucleus pulposus (NP) annulus fibrosus (AF) degeneration. We analyzed gene expression profiles of NP AF from Gene Expression Omnibus database. The differentially expressed (FRDEGs) degenerated were filtered, followed by GO KEGG analysis. Feature FRDEGs identified LASSO SVM-RFE algorithms, then Set Enrichment Analysis (GSEA) Variation (GSVA) conducted. Immune infiltration analysis was conducted CIBERSORT algorithm. established drug networks via Drug-Gene Interaction Database competitive endogenous RNA (ceRNA) miRanda, miRDB, TargetScan levels feature assessed validation sets, single-cell RNA-seq, experimental verification. A total 15 18 obtained AF, respectively. revealed their implication oxidative stress. Four (AKR1C1, AKR1C3, MUC1, ENPP2) five (SCP2, ABCC1, KLF2, IDO1, CREB3) GSEA GSVA showed that these enriched lots biological functions, including immune response. CREB3 negatively correlated with Eosinophils drugs ceRNAs targeting MUC1 identified. Experimental verification RNA-seq downregulated considered novel biomarkers ferroptosis, Drug ceRNA constructed future development investigation new mechanisms ferroptosis.

Язык: Английский

Selenoprotein K at the intersection of cellular pathways

Archives of Biochemistry and Biophysics, Год журнала: 2024, Номер unknown, С. 110221 - 110221

Опубликована: Ноя. 1, 2024

Язык: Английский