ArticleJournal of diabetes investigation2022
Activation of complement C1q and C3 in glomeruli might accelerate the progression of diabetic nephropathy: Evidence from transcriptomic data and renal histopathology.
Article in Journal of diabetes investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Polyunsaturated Fatty Acids and Diabetic Kidney Disease: What have We Learned so Far?Current nutrition reports · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Targeting Complement Component 1q Ameliorates Diabetic Endothelial Inflammation Via Orphan Nuclear Receptor 4a1-Dependent Suppression of Nuclear Factor κB Signaling.Journal of the American Heart Association · 2026Article
- Identification of Common Genes Regulated by ER Stress During the Development of Diabetic Nephropathy Based on Human Transcriptome Datasets and an In Vivo Mouse Model.International journal of molecular sciences · 2026Article
- Complement role in kidney disease: a comprehensive review and therapeutic innovations.BMC nephrology · 2026Review
- Article
- Multiomics Integration Analysis Reveals the Regulatory Mechanisms of Efferocytosis in Diabetic Kidney Disease.Inflammation · 2026Article
- Mechanisms of diabetic kidney disease and established and emerging treatments.Nature reviews. Endocrinology · 2026Review
- Complement System-Related Genes in Diabetic Nephropathy: Screening for Potential Targets of the Mechanism.Journal of diabetes research · 2026Article
- The Role of Complement Activation in Diabetic Nephropathy: Current Insights and Future Directions.Journal of clinical medicine · 2025Review
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Identification of potential therapeutic targets for complement-associated glomerular diseases using Mendelian randomization.Medicine · 2025Article
- Complement pathway: Risk molecular pattern of cardiovascular diseases in patients with diabetic nephropathy.Journal of medical biochemistry · 2025Article
- Complement anaphylatoxins: Potential therapeutic target for diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Complement classical and alternative pathway activation contributes to diabetic kidney disease progression: a glomerular proteomics on kidney biopsies.Scientific reports · 2025Article
- Integrated multi-omics with machine learning to uncover the intricacies of kidney disease.Briefings in bioinformatics · 2024Review
- Pathological mechanism of immune disorders in diabetic kidney disease and intervention strategies.World journal of diabetes · 2024Review
- Complement Cascade Proteins Correlate with Fibrosis and Inflammation in Early-Stage Type 1 Diabetic Kidney Disease in the Ins2Akita Mouse Model.International journal of molecular sciences · 2024Article
- VCAM1: an effective diagnostic marker related to immune cell infiltration in diabetic nephropathy.Frontiers in endocrinology · 2024Article
- The role of complement in kidney disease.Nature reviews. Nephrology · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
AIMS/
introductionIt is not unclear whether the complement system is involved in the pathogenesis of diabetic nephropathy (DN). We explored the role of the complement system in glomeruli from patients with DN using integrated transcriptomic bioinformatics analysis and renal histopathology. MATERIALS AND
methodsFour datasets (GSE30528, GSE104948, GSE96804 and GSE99339) from the Gene Expression Omnibus database were integrated. We used a protein-protein interaction network and the Molecular Complex Detection App to obtain hub genes. Gene ontology and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were carried out to identify significant pathways. We also investigated the associations of C1q and C3 deposition on renal histopathology with clinical data, pathological parameters and renal survival in DN patients.
resultsWe identified 47 up- and 48 downregulated genes associated with DN. C3, C1QB and C1QA were found to be complement-related hub genes. The gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses identified complement activation and humoral immune response as the significant oncology terms, with C1QB and C3 positioned at the center of the pathway. Regarding renal histopathology, patients with both C1q and C3 deposition had more severe glomerular classes. Multivariate Cox proportional hazards regression showed that the deposition of glomerular C1q and C3 was an independent risk factor for kidney failure. Patients with high C1q, C3 or C4d expression in glomeruli were more likely to progress to kidney failure, whereas glomerular mannose-binding lectin was rare.
conclusionsComplement activation is involved in the development of DN, and activation of the classical complement pathway in glomeruli might accelerate disease progression.
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