ReviewFrontiers in immunology2021
NLRP3 Inflammasome in Metabolic-Associated Kidney Diseases: An Update.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Associations between lipid metabolism and Henoch-Schönlein purpura nephritis in children: a systematic review and meta-analysis.Italian journal of pediatrics · 2026Pooled it
- Integrative transcriptomic and machine learning analysis identifies PYCARD and IFI30 as immune-lysosomal biomarkers of ANCA-associated glomerulonephritis.Renal failure · 2026Article
- Article
- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Imidacloprid induces hepatorenal toxicity in male albino rats via oxidative, immune inflammatory, and proliferative effects: a 90-day study.Scientific reports · 2026Article
- Resolving Inflammation in CKD: The Potential of SPMs and Omega-3 Derivatives as Biomarkers and Therapeutics.Biomedicines · 2026Review
- Tissue Expression of NLRP3, IL-1β, and IL-18 in Glomerular and Interstitial Inflammation Associated With Diabetic Nephropathy.Mediators of inflammation · 2026Article
- Immunological and inflammatory responses in the kidneys in experimental acanthamoebiasis.Microbiology spectrum · 2025Article
- Phosphodiesterase 4 Inhibition in Neuropsychiatric Disorders Associated with Alzheimer's Disease.Cells · 2025Review
- ATP/P2X7 receptor/NLRP3 pathway facilitates renal tubular epithelial-myofibroblast transdifferentiation and interstitial fibrosis in rats with unilateral ureteral obstruction.Frontiers in pharmacology · 2025Article
- Association between uric acid to high-density lipoprotein cholesterol ratio and chronic kidney disease in Chinese patients with type 2 diabetes mellitus: a cross-sectional study.Frontiers in nutrition · 2025Article
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- Long-Term Protective Effects and Mechanisms of Gastric Bypass Surgery on the Kidneys in Hypertensive Obese Rat.Obesity surgery · 2024Article
- Inulin Reduces Kidney Damage in Type 2 Diabetic Mice by Decreasing Inflammation and Serum Metabolomics.Journal of diabetes research · 2024Article
- Exploring the role of NLRP3 inflammasome in diabetic nephropathy and the advancements in herbal therapeutics.Frontiers in endocrinology · 2024Review
- Comprehensive analysis of the relationship between xanthine oxidoreductase activity and chronic kidney disease.iScience · 2023Article
- C/EBPβ-TFAM-Mediated NLRP3 Inflammasome Activation Contributes to Arsenic-Induced Rat Kidney Injury.Toxics · 2023Article
- Review
- Peroxiredoxin-4 and Dopamine D5 Receptor Interact to Reduce Oxidative Stress and Inflammation in the Kidney.Antioxidants & redox signaling · 2023Article
- Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic syndrome (MS) is a group of complex metabolic disorders syndrome, which refers to the pathological state of metabolism disorder of protein, fat, carbohydrate and other substances in human body. The kidney is an important organ of metabolism, and various metabolic disorders can lead to the abnormalities in the structure and function of the kidney. The recognition of pathogenesis and treatment measures of renal damage in MS is a very important part for the renal function preserve. Inflammatory response caused by various metabolic factors is a protective mechanism of the body, but persistent inflammation will become a harmful factor and aggravate kidney damage. Inflammasomes are sensors of the innate immune system that play crucial roles in initiating inflammation in response to acute infections and chronic diseases. They are multiprotein complex composed of cytoplasmic sensors (mainly NLR family members), apoptosis-associated speck-like protein (ASC or PYCARD) and pro-caspase-1. After receiving exogenous and endogenous stimuli, the sensors begin to assemble inflammasome and then promote the release of inflammatory cytokines IL-1β and IL-18, resulting in a special way of cell death named pyroptosis. In the kidney, NLRP3 inflammasome can be activated by a variety of pathways, which eventually leads to inflammatory infiltration, renal intrinsic cell damage and renal function decline. This paper reviews the function and specific regulatory mechanism of inflammasome in kidney damage caused by various metabolic disorders, which will provide a new therapeutic perspective and targets for kidney diseases.
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.