ArticleJournal of the American Society of Nephrology : JASN2017
A Heterologous Model of Thrombospondin Type 1 Domain-Containing 7A-Associated Membranous Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 82 citations in OpenAlex.
- Targeting tissue immune memory in chronic-remitting autoimmune kidney diseases: current concepts and future therapies.Clinical kidney journal · 2026Review
- Animal models of idiopathic membranous nephropathy: Recent advances and future perspectives.Animal models and experimental medicine · 2026Review
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- Secreted exosomes induce filopodia formation.eLife · 2026Article
- Contemporary review of primary membranous nephropathy.Frontiers in immunology · 2026Review
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Spontaneous remission in primary membranous nephropathy: mechanisms, predictive factors, and implications for personalized management.Frontiers in immunology · 2025Review
- THSD7A as a Promising Biomarker for Membranous Nephrosis.Molecular biotechnology · 2024Review
- THSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.Frontiers in pharmacology · 2024Article
- Animal models of membranous nephropathy: more choices and higher similarity.Frontiers in immunology · 2024Review
- The fate of immune complexes in membranous nephropathy.Frontiers in immunology · 2024Review
- The thickness of glomerular basement membrane predicts complete remission in primary membranous nephropathy.Renal failure · 2023Article
- Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis.Nature communications · 2023Article
- The classical pathway triggers pathogenic complement activation in membranous nephropathy.Nature communications · 2023Article
- Kidney diseases.Immunological reviews · 2023Review
- Containing anti-PLA2R IgG antibody induces podocyte injury in idiopathic membranous nephropathy.Renal failure · 2023Article
- C5b-9 Glomerular Deposits Are Associated With Poor Renal Survival in Membranous Nephropathy.Kidney international reports · 2023Article
- Membranous nephropathy: new pathogenic mechanisms and their clinical implications.Nature reviews. Nephrology · 2022Review
- The Alternative Pathway Is Necessary and Sufficient for Complement Activation by Anti-THSD7A Autoantibodies, Which Are Predominantly IgG4 in Membranous Nephropathy.Frontiers in immunology · 2022Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombospondin type 1 domain-containing 7A (THSD7A) is a target for autoimmunity in patients with membranous nephropathy (MN). Circulating autoantibodies from patients with THSD7A-associated MN have been demonstrated to cause MN in mice. However, THSD7A-associated MN is a rare disease, preventing the use of patient antibodies for larger experimental procedures. Therefore, we generated antibodies against the human and mouse orthologs of THSD7A in rabbits by coimmunization with the respective cDNAs. Injection of these anti-THSD7A antibodies into mice induced a severe nephrotic syndrome with proteinuria, weight gain, and hyperlipidemia. Immunofluorescence analyses revealed granular antigen-antibody complexes in a subepithelial location along the glomerular filtration barrier 14 days after antibody injection, and immunohistochemistry for rabbit IgG and THSD7A as well as ultrastructural analyses showed the typical characteristics of human MN. Mice injected with purified IgG from rabbit serum that was taken before immunization failed to develop any of these changes. Notably, MN developed in the absence of detectable complement activation, and disease was strain dependent.
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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 OpenQuestion graph.