ArticleFrontiers in medicine2022
Activation of Complement Pathways in Kidney Tissue May Mediate Tubulointerstitial Injury in Diabetic Nephropathy.
Article in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Curcumin attenuates high glucose-induced apoptosis in renal tubular epithelial cells by enhancing the Nrf2/heme oxygenase-1 antioxidant pathway.World journal of nephrology · 2026Article
- Multiomics Integration Analysis Reveals the Regulatory Mechanisms of Efferocytosis in Diabetic Kidney Disease.Inflammation · 2026Article
- The Role of Complement Activation in Diabetic Nephropathy: Current Insights and Future Directions.Journal of clinical medicine · 2025Review
- Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.Clinical kidney journal · 2024Review
- 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
- Review
- The Complement System in Kidney Transplantation.Cells · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Introduction: Key genes involved in tubulointerstitial injury may influence the development and progression of diabetic nephropathy (DN). We investigated whether complement-related genes are linked to the mechanism underlying tubulointerstitial injury in DN. Methods: We analyzed the microarray data of 17 tubulointerstitial tissue samples from DN patients and 21 normal controls from the Gene Expression Omnibus. A gene co-expression network was constructed, and genes were divided into modules by weighted gene co-expression network analysis (WGCNA). We also investigated the association of C3 and C1q deposits in kidney tissues with a composite outcome of end-stage renal disease or a 50% reduction in the estimated glomerular filtration rate (eGFR) in DN patients. Finally, we performed immunohistochemical analyses of C3, C1q, C5b-9, mannose-binding lectin (MBL), and factor B in kidney tissues. Results: Nine co-expression modules were constructed using 12,075 genes from the 38 human tubulointerstitial tissue samples. Black module with more genes was positively correlated with tubulointerstitial injury in DN. C3, one of the top 10 genes in tubulointerstitial injury, was verified in an independent dataset; C3 was significantly overexpressed in tubulointerstitial tissue from patients with DN compared to the normal controls. The mRNA level of C3 in renal tubulointerstitium was negatively correlated with eGFR in DN patients ( Conclusion: Local complement activation of the classical, lectin and alternative pathways appears linked to tubulointerstitial injury and disease progression in DN.
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