ArticleScientific reports2017
NLRP3 inflammasome: Pathogenic role and potential therapeutic target for IgA nephropathy.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 75 citations in OpenAlex.
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- Role of Omega-3 Fatty Acids in IgA Nephropathy: An Updated Review of Mechanisms and Evidence.Journal of clinical medicine · 2026Review
- Uromodulin p.His36Tyr promotes macrophage pyroptosis via App-Cd74 signaling to drive renal inflammation in ADTKD.Nature communications · 2026Article
- Review
- Differential Cell-Specific, Regulatory Roles of Fc γ Receptor IIB through IgG in IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- Hydroxychloroquine sulfate for IgA nephropathy: mechanisms and therapeutic potential in improving proteinuria and alleviating disease progression - a literature review.BMC nephrology · 2025Review
- Anti-Inflammatory Potential of Essential Oil from the Heart-Wood of the Folk Medicinal TreeInternational journal of molecular sciences · 2025Article
- A new era in the treatment of kidney diseases: NLRP3 inflammasome and cytokine-targeted therapies.Pediatric nephrology (Berlin, Germany) · 2025Review
- C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Multi-modal investigation reveals pathogenic features of diverse DDX3X missense mutations.PLoS genetics · 2025Article
- AIP1 Regulates Ocular Angiogenesis Via NLRP12-ASC-Caspase-8 Inflammasome-Mediated Endothelial Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Therapy Targeted to the NLRP3 Inflammasome in Chronic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Ferroptosis-Related Genes in IgA Nephropathy: Screening for Potential Targets of the Mechanism.International journal of genomics · 2024Article
- Research Progress of Pyroptosis in Renal Diseases.Current medicinal chemistry · 2024Review
- Autoinflammatory diseases and the kidney.Immunologic research · 2023Review
- Role of cuproptosis in understanding diseases.Human cell · 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
10 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously showed that IL-1β is involved in the pathogenesis of both spontaneously occurring and passively induced IgA nephropathy (IgAN) models. However, the exact causal-relationship between NLRP3 inflammasome and the pathogenesis of IgAN remains unknown. In the present study, we showed that [1] IgA immune complexes (ICs) activated NLRP3 inflammasome in macrophages involving disruption of mitochondrial integrity and induction of mitochondrial ROS, bone marrow-derived dendritic cells (BMDCs) and renal intrinsic cells; [2] knockout of NLRP3 inhibited IgA ICs-mediated activation of BMDCs and T cells; and [3] knockout of NLRP3 or a kidney-targeting delivery of shRNA of NLRP3 improved renal function and renal injury in a mouse IgAN model. These results strongly suggest that NLRP3 inflammasome serves as a key player in the pathogenesis of IgAN partly through activation of T cells and mitochondrial ROS production and that a local, kidney-targeting suppression of NLRP3 be a therapeutic strategy for IgAN.
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.