ReviewPflugers Archiv : European journal of physiology2017
A podocyte view of membranous nephropathy: from Heymann nephritis to the childhood human disease.
Review in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Spontaneous remission in primary membranous nephropathy: mechanisms, predictive factors, and implications for personalized management.Frontiers in immunology · 2025Review
- Membranous nephropathy: pathogenesis and treatments.MedComm · 2024Review
- ADAM10-Mediated Ectodomain Shedding Is an Essential Driver of Podocyte Damage.Journal of the American Society of Nephrology : JASN · 2021Article
- Triptolide ameliorates fine particulate matter-induced podocytes injury via regulating NF-κB signaling pathway.BMC molecular and cell biology · 2020Article
- How Does Herbal Medicine Treat Idiopathic Membranous Nephropathy?Frontiers in pharmacology · 2020Review
- A glomerulus-on-a-chip to recapitulate the human glomerular filtration barrier.Nature communications · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membranous nephropathy (MN) is characterized by an accumulation of immune deposits on the subepithelial side of the glomerular basement membrane, which results in complement activation and proteinuria. Since 2002, several major antigens of the podocyte have been identified in human MN, the first one being neutral endopeptidase (NEP), the alloantigen involved in neonatal cases of MN that occur in newborns from NEP-deficient mothers. This discovery opened the field to the major advances that have occurred since then in the pathophysiology and treatment of MN. It is remarkable that experimental models such as Heymann nephritis and cationic bovine serum albumin-induced MN in the rabbit predicted the pathomechanisms of the human glomerulopathy. The podocyte is at the center of the pathogenesis of MN either by providing a source of endogenous antigens or by creating an environment favorable to deposition and accumulation of immune complexes containing exogenous (non-podocyte) antigens. The podocyte is also a victim of complement activation and antibody blocking activity against enzymes or receptors. A search for innovative drugs aimed at protecting this cell against complement activation and the effects of prolonged ER stress has become a priority.
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Registered trials
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