ArticleAmerican journal of nephrology2015
Renal C3 complement component: feed forward to diabetic kidney disease.
Article in American journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed.
- Empagliflozin alleviates lipid deposition and inflammation in diabetic kidney disease by downregulating C1QC.Molecular and cellular biochemistry · 2026Article
- Complement System-Related Genes in Diabetic Nephropathy: Screening for Potential Targets of the Mechanism.Journal of diabetes research · 2026Article
- Shared immune-inflammatory gene networks and drug prediction in polycystic ovary syndrome and type 2 diabetes mellitus: a bioinformatics and experimental validation study.Frontiers in endocrinology · 2026Article
- C3a/C3aR axis is involved in diabetic kidney injury by regulating podocyte mitophagy in diabetic nephropathy.International journal of molecular medicine · 2025Article
- Identification of hub genes in the crosstalk between type 2 diabetic nephropathy and obesity according to bioinformatics analysis.Adipocyte · 2024Article
- 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
- Identification of transcription factors related to diabetic tubulointerstitial injury.Journal of translational medicine · 2023Article
- An in vitro approach to understand contribution of kidney cells to human urinary extracellular vesicles.Journal of extracellular vesicles · 2023Article
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- Association between serum complements and kidney function in patients with diabetic kidney disease.Frontiers in endocrinology · 2023Article
- Identification and validation of disulfidptosis-related gene signatures and their subtype in diabetic nephropathy.Frontiers in genetics · 2023Article
- Human complement component C3 N-glycome changes in type 1 diabetes complications.Frontiers in endocrinology · 2023Article
- Identification of key genes and miRNAs related to polycystic ovary syndrome by comprehensive analysis of microarray.BMC medical genomics · 2022Article
- Role of coagulation in persistent renal ischemia following reperfusion in an animal model.American journal of physiology. Renal physiology · 2022Article
- High-Throughput Human Complement C3 N-Glycoprofiling Identifies Markers of Early Onset Type 1 Diabetes Mellitus in Children.Molecular & cellular proteomics : MCP · 2022Article
- The Complement Pathway: New Insights into Immunometabolic Signaling in Diabetic Kidney Disease.Antioxidants & redox signaling · 2022Review
- Genetic Cross-Talk between Oral Squamous Cell Carcinoma and Type 2 Diabetes: The Potential Role of Immunity.Disease markers · 2022Article
- Identification of fibronectin 1 (FN1) and complement component 3 (C3) as immune infiltration-related biomarkers for diabetic nephropathy using integrated bioinformatic analysis.Bioengineered · 2021Article
- Complement factor B in high glucose-induced podocyte injury and diabetic kidney disease.JCI insight · 2021Article
- Investigation of the Mechanism of Complement System in Diabetic Nephropathy via Bioinformatics Analysis.Journal of diabetes research · 2021Article
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.
Funding
Abstract
backgroundDiabetic nephropathy is the main cause of end-stage renal disease and has reached epidemic proportions.
methodsComprehensive genomic profiling (RNAseq) was employed in the ZS (F1 hybrids of Zucker and spontaneously hypertensive heart failure) model of diabetic nephropathy. Controls were lean littermates.
resultsDiabetic nephropathy in obese, diabetic ZS was accelerated by a single episode of renal ischemia (DI). This rapid renal decline was accompanied by the activation of the renal complement system in DI, and to a lesser extent in sham-operated diabetic rats (DS). In DI there were significant increases in renal mRNA encoding C3, C4, C5, C6, C8, and C9 over sham-operated lean normal controls (LS). Moreover, mRNAs encoding the receptors for the anaphylatoxins C3a and C5a were also significantly increased in DI compared to LS. The classic complement pathway was activated in diabetic kidneys with significant increases of C1qa, C1qb, and C1qc mRNAs in DI over LS. In addition, critical regulators of complement activation were significantly attenuated in DI and DS. These included mRNAs encoding CD55, decay accelerating factor, and CD59, which inhibit the membrane attack complex. C3, C4, and C9 proteins were demonstrated in renal tubules and glomeruli. The complement RNAseq data were incorporated into a gene network showing interactions among C3-generating renal tubular cells and other immune competent migratory cells.
conclusionsWe conclude that local activation of the complement system mediates renal injury in diabetic nephropathy.
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.