ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2022
Expression of Ferroptosis-Related Genes is Correlated with Immune Microenvironment in Diabetic Kidney Disease.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mapping the future: bibliometric insights into ferroptosis and diabetic nephropathy.Frontiers in physiology · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Identification of Ferroptosis-Related Genes Associated With Cryptorchidism via Bioinformatics and Experimental Verification.Genetics research · 2025Article
- The research trends of ferroptosis in diabetes: a bibliometric analysis.Frontiers in public health · 2024Article
- Integrated Analysis of Ferroptosis and Immunity-Related Genes Associated with Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
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Authors and funding
5 authors.
Funding
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Abstract
Objective: This study aims to explore the correlation between ferroptosis and immune microenvironment (IME) in diabetic kidney disease (DKD) to provide a new clue for exploring the underlying molecular mechanisms. Methods: Corresponding RNA data of DKD patients were downloaded from GEO databases. The weighted gene co-expression network analysis (WGCNA) was used to construct the network, and the selected hub genes, then, overlapped with ferroptosis-related genes (FRGs) from FerrDb. Consensus clustering was performed to identify new molecular subgroups. ESTIMATE, TIMER and ssGSEA analyses were applied to determinate the IME and immune status. Functional analyses including GO, KEGG and GSEA were conducted to elucidate the underlying mechanisms. Results: Two molecular subtypes were identified based on the expression of FRGs. ESTIMATE algorithm revealed that there were significant differences in ESTIMATE score between these two clusters of DKD patients, with no significant difference found in stromal score and immune score. In addition, TIMER algorithm indicated there was a significant difference in the degree of T cell infiltration. The ssGSEA algorithm showed immunity was mainly concentrated in thick ascending limb and distal convoluted tubule in adult kidney. GO, KEGG and GSEA analyses revealed that the differentially expressed genes (DEGs) were mainly enriched in immune and metabolism associated pathways. Conclusion: The ferroptosis may be induced by dysregulation of IME, thereby accelerating the progression of DKD. Our work could be applied to provide a new clue for exploring the underlying molecular mechanisms and sheds novel light on the therapy strategy of DKD.
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