ArticleThe American journal of pathology1996
Lipoproteins accumulate in immune deposits and are modified by lipid peroxidation in passive Heymann nephritis.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed.
- Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026Review
- Towards the Definition of the Molecular Hallmarks of Idiopathic Membranous Nephropathy in Serum Proteome: A DIA-PASEF Approach.International journal of molecular sciences · 2023Article
- Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis.Nature communications · 2023Article
- C5b-9 Glomerular Deposits Are Associated With Poor Renal Survival in Membranous Nephropathy.Kidney international reports · 2023Article
- Lysosome function in glomerular health and disease.Cell and tissue research · 2021Review
- Alterations in the ubiquitin proteasome system in persistent but not reversible proteinuric diseases.Journal of the American Society of Nephrology : JASN · 2014Article
- Pathogenic antibodies inhibit the binding of apolipoproteins to megalin/gp330 in passive Heymann nephritis.The Journal of clinical investigation · 1997Article
- Identification of the second cluster of ligand-binding repeats in megalin as a site for receptor-ligand interactions.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Proteinuria in passive Heymann nephritis is primarily caused by reactive oxygen species that are produced by glomerular cells. Reactive oxygen species apparently exert their damaging effects on the glomerular filter by lipid peroxidation and subsequent adduct formation on matrix proteins of glomerular basement membranes. This raised the question as to the source of polyunsaturated fatty acids required as substrates for lipid peroxidation. Here we have localized by immunocytochemistry rat apolipoprotein E and apolipoprotein B within subepithelial immune deposits. Moreover, apolipoprotein B extracted from isolated glomeruli of proteinuric passive Heymann nephritis rats shows degradation and lipid peroxidation adduct formation, similar to apoproteins of oxidized lipoproteins in atherosclerotic lesions. These data provide evidence that lipoproteins accumulate within immune deposits and suggest that their lipids generate lipid-peroxidation-derived reactive compounds.
Indexed as
Identifiers
8863678PMC1865180What OpenQuestion holds
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.