ReviewRenal failure2022
Research progress on related mechanisms of uric acid activating NLRP3 inflammasome in chronic kidney disease.
Review in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- A holistic guide to effective prevention and treatment for kidney stones: a systematic review exploring anti-urolithiasis approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2026Pooled it
- Urate-lowering therapy modifies associations between urinary urate and kidney outcome.Renal failure · 2026Article
- The Nonlinear Relationship Between Serum Uric Acid and Cardiovascular Disease Risk: Mechanistic Insights and Clinical Implications.Cardiovascular drugs and therapy · 2026Review
- NLRP3 inflammasome activation by particles and fibers: implications for human hazard assessment.Archives of toxicology · 2026Review
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- Article
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.Experimental physiology · 2026Article
- Exploring the mechanisms of serum miRNA in obesity-related kidney injury.International urology and nephrology · 2026Review
- Purine-Metabolism Reprogramming Associated with Failed-Repair Proximal Tubule States in the AKI-to-CKD Transition.Metabolites · 2026Article
- Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.Journal of advanced research · 2026Review
- [Small intestinal bacterial overgrowth and inflammatory factor expression levels in patients with asymptomatic hyperuricemia].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- Renin-Independent Aldosteronism Heightened the Risk of Renal Impairment in Chinese Adults From Hakka Biobank.Kidney medicine · 2026Article
- Synergistic Impact of Fasting Plasma Glucose and Serum Uric Acid on Peripheral Diabetic Retinopathy Severity in T2DM Patients.Translational vision science & technology · 2026Article
- Observational
- Network Pharmacology and Transcriptomic Analysis Reveal the Therapeutic Mechanisms of Xiebai Bining Decoction in Hyperuricemic Nephropathy.Combinatorial chemistry & high throughput screening · 2026Article
- Association between triglyceride-to-high-density lipoprotein cholesterol ratio and albuminuria in patients with type 2 diabetes: a cross-sectional study.Frontiers in nutrition · 2026Article
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
- Association between hyperuricemia and kidney stones in Southern China: a multicentre cross-sectional study.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperuricemia is an independent risk factor for the progression of chronic kidney disease. High levels of uric acid can lead to a series of pathological conditions, such as gout, urinary stones, inflammation, and uric acid nephropathy. There is a close relationship between uric acid and the NLRP3 inflammasome. NLRP3 inflammasome activation can cause cell damage and even death through endoplasmic reticulum stress, lysosome destruction, mitochondrial dysfunction, and the interaction between the Golgi apparatus and extracellular vesicles. In addition, the NLRP3 inflammasome acts as a molecular platform, triggering the activation of caspase-1 and the lysis of IL-1β, IL-18 and Gasdermin D (GSDMD) through different molecular mechanisms. Cleaved NT-GSDMD forms pores in the cell membrane and triggers pyrophosphorylation, thereby inducing cell death and releasing many intracellular proinflammatory molecules. In recent years, studies have found that hyperuricemia or uric acid crystals can activate NLRP3 inflammasomes, and the activation of NLRP3 inflammasomes plays an important role in kidney disease. This article reviews the possible pathophysiological mechanisms by which uric acid activates inflammasomes and induces kidney damage at the cellular and molecular levels.
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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.