ArticleBMC medical genomics2023
Identification and validation of immune-related biomarkers and potential regulators and therapeutic targets for diabetic kidney disease.
Article in BMC medical genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The Impact of the Alternate Mediterranean Diet (aMED) on the Prevention of Chronic Liver Disease: A Meta-Analysis of Observational Studies.Nutrients · 2025Pooled it
- Systematic cell-type resolved transcriptomes of 8 tissues in 8 lab and wild-derived mouse strains capture global and local expression variation.Cell genomics · 2026Article
- Diagnostic and prognostic signatures of glomerular membrane dysregulation in immune nephropathies.Frontiers in immunology · 2026Article
- Integrative transcriptomic and genomic insights into diabetic kidney disease: evidence from multi-omics analysis and experimental validation.Renal failure · 2025Article
- FGF9 alleviates diabetic cardiomyopathy by activating Nrf2 via SQSTM1/p62-Keap1 in mice.Communications biology · 2025Article
- Reduced FGF9 Leads to Kidney Injury Through Regulating Renal Tubular Epithelial Cell EMT in Diabetes.Journal of cellular and molecular medicine · 2025Article
- Fyn Kinase: A Potential Target in Glucolipid Metabolism and Diabetes Mellitus.Current issues in molecular biology · 2025Review
- Tracing the molecular landscape of diabetic nephropathy: Insights from machine learning and experiment verification.Journal of diabetes investigation · 2025Article
- Exploring the interplay between adipokine-mediated celastrol target genes and T cells in diabetic nephropathy: a mendelian randomization-based causal inference.Diabetology & metabolic syndrome · 2025Article
- Celastrol protects against diabetic nephropathy by modulating immune-related pathways: a bioinformatics and experimental validation.American journal of translational research · 2025Article
- A genotype-guided prediction model for the incidence of persistent acute kidney injury following lung transplantation.BMC nephrology · 2024Article
- Atherogenic Index of Plasma as an Early Marker of Chronic Kidney Disease and Liver Injury in Type 2 Diabetes.Clinical medicine insights. Endocrinology and diabetes · 2024Article
- Uncovering the mechanism of resveratrol in the treatment of diabetic kidney disease based on network pharmacology, molecular docking, and experimental validation.Journal of translational medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic kidney disease (DKD) is a major complication of diabetes and the leading cause of end-stage renal disease worldwide. Renal inflammation and infiltration of immune cells contribute to the development and progression of DKD. Thus, the aim of the present study was to identify and validate immune-related biomarkers and analyze potential regulators including transcription factors (TFs), microRNAs (miRNAs), and drugs for DKD.
methodsImmune-related genes from the ImmPort database and glomeruli samples from GSE1009 and GSE30528 were used to identify differentially expressed immune-related genes (DEIRGs) of DKD. The expression level and clinical correlation analyses of DEIRGs were verified in the Nephroseq database. Murine podocytes were cultured to construct the high glucose-induced podocyte injury model. The reliability of the bioinformatics analysis was experimentally validated by RT-qPCR in podocytes. Networks among DEIRGs, regulators, and drugs were constructed to predict potential regulatory mechanisms for DKD.
resultsDKD-associated DEIRGs were identified. CCL19 and IL7R were significantly upregulated in the DKD group and negatively correlated with glomerular filtration rate (GFR). GHR, FGF1, FYN, VEGFA, F2R, TGFBR3, PTGDS, FGF9, and SEMA5A were significantly decreased in the DKD group and positively correlated with GFR. RT-qPCR showed that the relative mRNA expression levels of GHR, FGF1, FYN, TGFBR3, PTGDS, FGF9, and SEMA5A were significantly down-regulated in the high glucose-induced podocyte injury group. The enriched regulators for DEIRGs included 110 miRNAs and 8 TFs. The abnormal expression of DEIRGs could be regulated by 16 established drugs.
conclusionsThis study identified immune-related biomarkers, regulators, and drugs of DKD. The findings of the present study provide novel insights into immune-related diagnosis and treatment of DKD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.