ReviewThe Journal of clinical investigation2025
Role of local complement activation in kidney fibrosis and repair.
Review in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- A four-gene signature for diagnosis of acute kidney injury following kidney transplantation.Renal failure · 2026Article
- Deletion of decay-accelerating factor in kidney tubular cells mitigates kidney fibrosis in aristolochic acid nephropathy.American journal of physiology. Renal physiology · 2026Article
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Urine Proteomic Profiling at Admission Reveals Complement Biomarkers Linked to Alcohol-Associated Liver Disease.Alcohol, clinical & experimental research · 2026Article
- Shifting From Systemic to Precision-Targeted Complement Therapies: Opportunities and Hurdles.European journal of immunology · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Cellular microenvironment of erythropoietin-producing cells in hypoxic and injured mouse kidneys.Experimental physiology · 2026Article
- Impact of hepatitis C therapy on urinary outcomes and renal function: a prospective real-world cohort study of early kidney changes.BMC nephrology · 2026Article
- Progressive endocannabinoid system dysregulation in autosomal dominant polycystic kidney disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Association of Urinary Complement Peptides with Kidney Function and Progression of Kidney Disease.International journal of molecular sciences · 2026Article
- Kidney-Lung Crosstalk in Acute Nephrologic Involvement: Mechanisms, Complement Activation, and Implications for Multiorgan Dysfunction.Life (Basel, Switzerland) · 2026Review
- Urinary complement C3 fragment levels and their clinical relevance in MPO-ANCA-associated vasculitis.Scientific reports · 2026Article
- Complement C5 inhibition in generalized myasthenia gravis is associated with improved survival and increased cardiovascular risk.Frontiers in immunology · 2026Article
- Eculizumab in C3 Glomerulopathy: A Systematic Review of Therapeutic Efficacy and Clinical Outcomes.Pharmaceutics · 2025Review
- Single-Cell and Spatial Transcriptomics in Renal Injury and Fibrosis Research.Kidney diseases (Basel, Switzerland)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is an important component of the innate immune system involved in host defense and maintaining homeostasis. While the liver is the main source of complement proteins in the bloodstream, recent research has shown that various tissues, including the kidneys, can produce complement components locally in response to both acute and chronic inflammation. This Review highlights evidence from animal models of glomerular and tubulointerstitial kidney disease showing increased expression of intracellular complement in the kidneys. Studies using knockout mice for complement and complement receptors, along with complement inhibitors, have demonstrated that reduced complement activation in animal models of kidney fibrosis led to reduced inflammation and fibrosis, thereby supporting the pathogenic role of complement activation. Data from single-cell RNA-sequencing, spatial transcriptomics, and proteomics studies further demonstrate that alterations in local complement levels contribute to the fibrotic microenvironment observed in these models. Additionally, kidney biopsy results from patients with acute kidney injury and chronic kidney disease (CKD) indicate an increased expression of intracellular complement components as disease progresses. Developing drugs aimed at diminishing the expression and activation of local complement in glomerular and tubulointerstitial kidney disease could provide a novel approach to managing CKD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.