ArticleNature communications2023
The classical pathway triggers pathogenic complement activation in membranous nephropathy.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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The trial behind it
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Who cites it
69 citing papers in PubMed, 89 citations in OpenAlex.
- Serum PLA2R-IgG4/PLA2R-IgG ratio dynamics reveal pathogenic autoantibody subclass switch during progression of PLA2R-associated membranous nephropathy.Annals of medicine · 2026Article
- Oral administration of ultrafine-grained Astragalus membranaceus enhances peripheral immunity in weaned black Xiangdong goats by upregulating the complement regulator C4bp and immunoglobulin responses.Molecular biology reports · 2026Article
- Distinct Complement Activation Profiles Between NELL1- and PLA2R-Associated Membranous Nephropathy: A Clinicopathological and Proteomic Study.Nephrology (Carlton, Vic.) · 2026Article
- FAT1-associated membranous nephropathy after hematopoietic stem cell transplantation: a case report and review of the literature.CEN case reports · 2026Review
- Human biomarker navigator.iMeta · 2026Review
- Emerging Immune Cell Biomarkers in Primary Membranous Nephropathy: Immune Cell Profiling During Anti-CD20 B Cell-Targeted Therapy.International journal of molecular sciences · 2026Review
- The Synthetic Melanocortin Agonist NDP-MSH Ameliorates THSD7A-Associated Membranous Nephropathy in an Active Immunization Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Animal models of idiopathic membranous nephropathy: Recent advances and future perspectives.Animal models and experimental medicine · 2026Review
- Transcriptomic analysis of differential expression and correlation of coding and non-coding RNAs in urine from patients with idiopathic membranous nephropathy.Biology direct · 2026Article
- Serum anti-PLA2R negativity does not exclude glomerular PLA2R expression in primary membranous nephropathy.Biomolecules & biomedicine · 2026Article
- Complement Profiling in Glomerular Disease: Insights from Laser Microdissection and Mass Spectrometry.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- C/EBP-β-regulated complement hyperactivation in spleen of SFTSV-infected mice: A clue to targeted complement therapy.PLoS pathogens · 2026Article
- Complement role in kidney disease: a comprehensive review and therapeutic innovations.BMC nephrology · 2026Review
- Complement-Mediated Kidney Diseases: Role of Alternative Pathway in Glomerular Inflammation.Kidney international reports · 2026Review
- Response mechanism of hepatorenal metabolic barrier function to drugs and environmental poisons and intervention strategy of natural products.Frontiers in pharmacology · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Complement and inflammasome crosstalk in chronic inflammation.Frontiers in immunology · 2026Review
- Contemporary review of primary membranous nephropathy.Frontiers in immunology · 2026Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membranous nephropathy (MN) is an antibody-mediated autoimmune disease characterized by glomerular immune complexes containing complement components. However, both the initiation pathways and the pathogenic significance of complement activation in MN are poorly understood. Here, we show that components from all three complement pathways (alternative, classical and lectin) are found in renal biopsies from patients with MN. Proximity ligation assays to directly visualize complement assembly in the tissue reveal dominant activation via the classical pathway, with a close correlation to the degree of glomerular C1q-binding IgG subclasses. In an antigen-specific autoimmune mouse model of MN, glomerular damage and proteinuria are reduced in complement-deficient mice compared with wild-type littermates. Severe disease with progressive ascites, accompanied by extensive loss of the integral podocyte slit diaphragm proteins, nephrin and neph1, only occur in wild-type animals. Finally, targeted silencing of C3 using RNA interference after the onset of proteinuria significantly attenuates disease. Our study shows that, in MN, complement is primarily activated via the classical pathway and targeting complement components such as C3 may represent a promising therapeutic strategy.
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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.