ReviewBiomedicines2023
Lupus Nephritis and Dysbiosis.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Systematic review of bidirectional interaction between gut microbiome, miRNAs, and human pathologies.Frontiers in microbiology · 2025Pooled it
- The landscape of cellular immune alteration in systemic lupus erythematosus.Frontiers in immunology · 2026Review
- The Gut Microbiota: Emerging Evidence in Autoimmune and Inflammatory Diseases.Research (Washington, D.C.) · 2026Review
- Review
- Endothelial cells regulate mesangial cells through the Dll4/Notch3 axis to participate in glomerular injury in lupus nephritis.Frontiers in immunology · 2026Article
- Artificial intelligence empowers gut microbiota research in neurodegenerative diseases molecular mechanisms and precision therapy.iScience · 2025Review
- Urine-Derived CD105-Positive Exosome Promotes Macrophage M1 Polarization Through the TGF-β1/Smad3 Signaling Axis To Exacerbate Lupus Nephritis.Inflammation · 2025Article
- Determining IFI44 as a key lupus nephritis's biomarker through bioinformatics and immunohistochemistry.Renal failure · 2025Article
- Inhibition of ferroptosis-related NCF2 blocks the progression of lupus nephritis by activating PPARα pathway.Hereditas · 2025Article
- Lupus Nephritis from Pathogenesis to New Therapies: An Update.International journal of molecular sciences · 2024Review
- Macrophages communicate with mesangial cells through the CXCL12/DPP4 axis in lupus nephritis pathogenesis.Cell death & disease · 2024Article
- The Disease with a Thousand Faces and the Human Microbiome-A Physiopathogenic Intercorrelation in Pediatric Practice.Nutrients · 2023Review
- Important denominator between autoimmune comorbidities: a review of class II HLA, autoimmune disease, and the gut.Frontiers in immunology · 2023Review
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
Lupus nephritis (LN) is one of the most common and serious complications of systemic lupus erythematosus (SLE). The risk factors for developing LN by SLE patients are not fully understood. They are considered to be a mix of genetic and environmental variables, one of them being dysbiosis, proposed recently to interfere with autoimmunity. As of yet, the relations between the human microbiome, its genetic determinants, individual variability and clinical consequences remain to be established. One of the major obstacles in studying them is the magnitude of confounders, such as diet, drugs, infections or antibiotics use. They also make comparison between the studies extremely complicated. We reviewed the available evidence for the interplay between microbiome, dysbiosis and mechanisms triggering the autoimmune responses and potentially contributing to LN development. One such mechanism is the stimulation of autoimmune responses by bacterial metabolites that can mimic autoantigens and cause antibody production. These mimicking microbial antigens seem to be a promising target for future interventions.
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.