ArticleThe Journal of experimental medicine2020
Loss of decay-accelerating factor triggers podocyte injury and glomerulosclerosis.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Nanotechnology-mediated podocyte injury repair: mechanistic exploration and therapeutic prospects.Renal failure · 2026Review
- Deletion of decay-accelerating factor in kidney tubular cells mitigates kidney fibrosis in aristolochic acid nephropathy.American journal of physiology. Renal physiology · 2026Article
- SnRNA-seq and genome-wide CRISPR screening define the complete transcriptional trajectory and functional drivers of podocyte stress.Cellular and molecular life sciences : CMLS · 2026Article
- Combined Anti-CD20/Anti-CD38 Therapy in Posttransplant Focal Segmental Glomerulosclerosis Recurrence: A Retrospective, International, Multicenter Study.Transplantation direct · 2026Article
- Multi-omics analyses demonstrate complement dysregulation is involved in focal segmental glomerulosclerosis.Frontiers in immunology · 2026Article
- C3a/C3aR axis is involved in diabetic kidney injury by regulating podocyte mitophagy in diabetic nephropathy.International journal of molecular medicine · 2025Article
- Complement and IgM in FSGS: Minor Characters or Leading Actors?Kidney360 · 2025Article
- The Influence of Anti-C3aR and Anti-C5aR Antibody Levels on the Course of Specific Glomerulonephritis Types.Journal of clinical medicine · 2025Article
- Complement Proteins Identify Rapidly Progressive Diabetic Kidney Disease.Kidney international reports · 2025Article
- Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025Review
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Clinical Significance of Immune Deposits and Complement System Activation in FSGS: Findings from the Cure Glomerulonephropathy Network Study.Kidney360 · 2025Article
- Pathogenesis of Focal Segmental Glomerulosclerosis and Minimal Change Disease: Insights from Glomerular Proteomics.Life (Basel, Switzerland) · 2025Article
- The Spectrum of Minimal Change Disease/Focal Segmental Glomerulosclerosis: From Pathogenesis to Proteomic Biomarker Research.International journal of molecular sciences · 2025Review
- To biopsy or not to biopsy a teenager with idiopathic nephrotic syndrome? Biopsy first.Pediatric nephrology (Berlin, Germany) · 2025Article
- Targeted Complement Treatments in Glomerulopathies: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Glucosyl Hesperidin Supplementation Prevents Tubulointerstitial Fibrosis and Immune Activation in Diabetic Nephropathy in Mice.Nutrients · 2025Article
- Human Adipose Tissue-Derived Stromal Cells Ameliorate Adriamycin-Induced Nephropathy by Promoting Angiogenesis.Organogenesis · 2024Article
- Proteomics and Incident Kidney Failure in Individuals With CKD: The African American Study of Kidney Disease and Hypertension and the Boston Kidney Biopsy Cohort.Kidney medicine · 2024Article
Corrections and comments
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Authors and funding
26 authors at 11 institutions in 4 countries.
Funding
Abstract
Kidney glomerulosclerosis commonly progresses to end-stage kidney failure, but pathogenic mechanisms are still poorly understood. Here, we show that podocyte expression of decay-accelerating factor (DAF/CD55), a complement C3 convertase regulator, crucially controls disease in murine models of adriamycin (ADR)-induced focal and segmental glomerulosclerosis (FSGS) and streptozotocin (STZ)-induced diabetic glomerulosclerosis. ADR induces enzymatic cleavage of DAF from podocyte surfaces, leading to complement activation. C3 deficiency or prevention of C3a receptor (C3aR) signaling abrogates disease despite DAF deficiency, confirming complement dependence. Mechanistic studies show that C3a/C3aR ligations on podocytes initiate an autocrine IL-1β/IL-1R1 signaling loop that reduces nephrin expression, causing actin cytoskeleton rearrangement. Uncoupling IL-1β/IL-1R1 signaling prevents disease, providing a causal link. Glomeruli of patients with FSGS lack DAF and stain positive for C3d, and urinary C3a positively correlates with the degree of proteinuria. Together, our data indicate that the development and progression of glomerulosclerosis involve loss of podocyte DAF, triggering local, complement-dependent, IL-1β-induced podocyte injury, potentially identifying new therapeutic targets.
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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.