ArticleFrontiers in pharmacology2024
THSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- 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
- Functional characterization of podocyte-expressed THSD7A in experimental membranous nephropathy.JCI insight · 2026Article
- Molecular immunopharmacology of traditional Chinese medicine-derived compounds in membranous nephropathy: mechanistic insights into immune aging and kidney essence deficiency.Frontiers in immunology · 2026Review
- Narrative review on decoding the crosstalk between lipid homeostasis and immune pathways in membranous nephropathy.BMC nephrology · 2025Review
- Urinary betaine/creatinine ratio enhances diagnostic accuracy of PLA2R-Ab in idiopathic membranous nephropathy.BMC nephrology · 2025Article
- Antigens in membranous nephropathy: discovery and clinical implications.Nature reviews. Nephrology · 2025Review
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Hemoglobin-associatedFrontiers in medicine · 2025Article
- Efficacy and safety of ripertamab for treating primary membranous nephropathy among adults: a multicenter, retrospective, real-world study.Frontiers in immunology · 2025Observational
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6 authors.
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Abstract
Membranous nephropathy (MN) continues to be a leading cause of nephrotic syndrome in non-diabetic adults. As a unique subtype in the serology-based classification of MN, thrombospondin type 1 domain containing 7A (THSD7A)-associated MN has attracted increasing interest, because, unlike other autoantigens, THSD7A is also expressed in preclinical species, facilitating the study of its role in MN. A heterologous mouse model of THSD7A-associated MN was previously established using a proprietary in-house antibody that was unfortunately not available to the research community. Here, we developed a mouse model of THSD7A-associated MN by administering a commercially available antibody targeting the most N-terminal part of THSD7A. Our model was characterized by heavy proteinuria and pathological features of human MN without sex differences. Complement depletion with cobra venom factor only partially attenuated proteinuria and glomerular injury in this model, entailing that complement-independent pathomechanisms also contribute. Consistently,
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