ReviewArthritis research & therapy2011
Chromatin as a target antigen in human and murine lupus nephritis.
Review in Arthritis research & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 27 citations in OpenAlex.
- Iron metabolism and ferroptosis: druggable targets to delay the progression of lupus nephritis.American journal of physiology. Renal physiology · 2026Review
- Circadian rhythms and renal pathophysiology.The Journal of clinical investigation · 2022Review
- 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
- Iron Metabolism: An Under Investigated Driver of Renal Pathology in Lupus Nephritis.Frontiers in medicine · 2021Review
- Mesoscale Modeling of Nucleosome-Binding Antibody PL2-6: Mono- versus Bivalent Chromatin Complexes.Biophysical journal · 2020Article
- Evaluation of the functional effects of genetic variants‒missense and nonsense SNPs, indels and copy number variations‒in the gene encoding human deoxyribonuclease I potentially implicated in autoimmunity.Scientific reports · 2019Article
- Parvovirus B19V Nonstructural Protein NS1 Induces Double-Stranded Deoxyribonucleic Acid Autoantibodies and End-Organ Damage in Nonautoimmune Mice.The Journal of infectious diseases · 2019Article
- Article
- What is damaging the kidney in lupus nephritis?Nature reviews. Rheumatology · 2016Review
- Molecular studies of lupus nephritis kidneys.Immunologic research · 2015Review
- Identification of the functional alleles of the nonsynonymous single-nucleotide polymorphisms potentially implicated in systemic lupus erythematosus in the human deoxyribonuclease I gene.DNA and cell biology · 2014Article
- The pathogenesis and diagnosis of systemic lupus erythematosus: still not resolved.Seminars in immunopathology · 2014Review
- Evaluation of all nonsynonymous single-nucleotide polymorphisms in the gene encoding human deoxyribonuclease I-like 1, possibly implicated in the blocking of endocytosis-mediated foreign gene transfer.DNA and cell biology · 2014Article
- The constant region contributes to the antigenic specificity and renal pathogenicity of murine anti-DNA antibodies.Journal of autoimmunity · 2012Article
- Mesangial cell-specific antibodies are central to the pathogenesis of lupus nephritis.Clinical & developmental immunology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present review focuses on pathogenic molecular and transcriptional events in patients with lupus nephritis. These factors are renal DNaseI, exposed chromatin fragments and the corresponding chromatin-reactive autoantibodies. Lupus nephritis is the most serious complication in human systemic lupus erythematosus, and is characterised by deposition of chromatin fragment-IgG complexes in the mesangial matrix and glomerular basement membranes. The latter deposition defines end-stage disease. This event is stringently linked to a renal-restricted shutdown of expression of the DNaseI gene, as determined by loss of DNaseI mRNA level and DNaseI enzyme activity. The major aim of the present review is to generate new therapeutic strategies based on new insight into the disease pathogenesis.
Indexed as
Identifiers
What 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.