ReviewMolecular medicine (Cambridge, Mass.)2013
Lupus nephritis: enigmas, conflicting models and an emerging concept.
Review in Molecular medicine (Cambridge, Mass.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Philosophical and distinct SLE epitomes: dogmas in conflict with evidences and an intellectual dissonance between established pathophysiological models.Frontiers in immunology · 2025Review
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- Regulation of chromatin architecture by protein binding: insights from molecular modeling.Biophysical reviews · 2024Review
- Why is it so difficult to understand why we don't understand human systemic lupus erythematosus? Contemplating facts, conflicts, and impact of "the causality cascade paradigm".Frontiers in immunology · 2024Review
- The greatest contribution to medical science is the transformation from studying symptoms to studying their causes-the unrelenting legacy of Robert Koch and Louis Pasteur-and a causality perspective to approach a definition of SLE.Frontiers in immunology · 2024Article
- SLE: a cognitive step forward-a synthesis of rethinking theories, causality, and ignored DNA structures.Frontiers in immunology · 2024Review
- Serum IgE anti-dsDNA autoantibodies in patients with proliferative lupus nephritis are associated with tubulointerstitial inflammation.Renal failure · 2023Article
- Anti-double stranded DNA antibodies: A rational diagnostic approach in limited-resource settings.Practical laboratory medicine · 2022Article
- SLE classification criteria: Science-based icons or algorithmic distractions - an intellectually demanding dilemma.Frontiers in immunology · 2022Article
- Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus.International journal of molecular sciences · 2021Article
- Comparisons of Anti-dsDNA Antibody Detection Methods by Chemiluminescent Immunoassay and Enzyme-Linked Immunosorbent Assay in Systemic Lupus Erythematosus.Diagnostics (Basel, Switzerland) · 2021Article
- The Anti-DNA Antibodies: Their Specificities for Unique DNA Structures and Their Unresolved Clinical Impact-A System Criticism and a Hypothesis.Frontiers in immunology · 2021Review
- Serum antinuclear antibodies associate with worse prognosis in AQP4-positive neuromyelitis optica spectrum disorder.Brain and behavior · 2021Article
- Kidney Tertiary Lymphoid Structures in Lupus Nephritis Develop into Large Interconnected Networks and Resemble Lymph Nodes in Gene Signature.The American journal of pathology · 2020Article
- Autoantibody-dependent amplification of inflammation in SLE.Cell death & disease · 2020Article
- Mesoscale Modeling of Nucleosome-Binding Antibody PL2-6: Mono- versus Bivalent Chromatin Complexes.Biophysical journal · 2020Article
- Evidence for a pathogenic role of extrafollicular, IL-10-producing CCR6Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The dsDNA, Anti-dsDNA Antibody, and Lupus Nephritis: What We Agree on, What Must Be Done, and What the Best Strategy Forward Could Be.Frontiers in immunology · 2019Review
- Lupus nephritis: low urinary DNase I levels reflect loss of renal DNase I and may be utilized as a biomarker of disease progression.The journal of pathology. Clinical research · 2018Article
- Systemic Lupus Erythematosus: Definitions, Contexts, Conflicts, Enigmas.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoantibodies to components of chromatin, which include double-stranded DNA (dsDNA), histones and nucleosomes, are central in the pathogenesis of lupus nephritis. How anti-chromatin autoantibodies exert their nephritogenic activity, however, is controversial. One model assumes that autoantibodies initiate inflammation when they cross-react with intrinsic glomerular structures such as components of membranes, matrices or exposed nonchromatin ligands released from cells. Another model suggests glomerular deposition of autoantibodies in complex with chromatin, thereby inducing classic immune complex-mediated tissue damage. Recent data suggest acquired error of renal chromatin degradation due to the loss of renal DNaseI enzyme activity is an important contributing factor to the development of lupus nephritis in lupus-prone (NZBxNZW)F1 mice and in patients with lupus nephritis. Down-regulation of DNaseI expression results in reduced chromatin fragmentation and in deposition of extracellular chromatin-IgG complexes in glomerular basement membranes in individuals who produce IgG anti-chromatin autoantibodies. The main focus of the present review is to discuss whether exposed chromatin fragments in glomeruli are targeted by potentially nephritogenic anti-dsDNA autoantibodies or if the nephritogenic activity of these autoantibodies is explained by cross-reaction with intrinsic glomerular constituents or if both models coexist in diseased kidneys. In addition, the role of silencing of the renal DNaseI gene and the biological consequences of reduced chromatin fragmentation in nephritic kidneys are discussed.
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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.