ArticleJournal of cellular and molecular medicine2020
Soluble uric acid induces myocardial damage through activating the NLRP3 inflammasome.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Inflammatory cytokines and immune signalling in heart failure: mechanisms, models, and emerging therapies.Cardiovascular research · 2026Review
- The Nonlinear Relationship Between Serum Uric Acid and Cardiovascular Disease Risk: Mechanistic Insights and Clinical Implications.Cardiovascular drugs and therapy · 2026Review
- Defective autophagy in diabetic nephropathy sensitizes podocytes to hyperuricemia induced injury by amplifying inflammasome activation.Clinical and experimental nephrology · 2026Article
- Isobavachin Attenuates Renal and Cardiac Injury in Chronic Hyperuricemia via Modulation of NF-κB and NLRP3 Signaling Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Association Between Serum Uric Acid and Pulmonary Hypertension in Takayasu Arteritis With Pulmonary Artery Involvement: A Cross-Sectional Study.Pulmonary circulation · 2026Article
- From uric acid to tophi: multistage molecular and cellular mechanisms of tophi formation.Frontiers in immunology · 2026Review
- Predictive Value of Uric Acid-to-Albumin Ratio for Left Atrial Thrombus or Spontaneous Echo Contrast in Patients with Non-Valvular Atrial Fibrillation.Journal of inflammation research · 2026Article
- From soluble uric acid to sodium urate crystal: immune metabolic inflammation driven by uric acid morphological transformation and mechanism-oriented therapy.Frontiers in immunology · 2026Review
- Hyperuricemia in Chronic Kidney Disease: Emerging Pathophysiology and a Novel Therapeutic Strategy.International journal of molecular sciences · 2025Review
- Effects of febuxostat on heart failure patients with asymptomatic hyperuricaemia: a retrospective cohort study.BMJ open · 2025Article
- Shikonin inhibits NLRP3 inflammasome activation and controls inflammatory disease.Scientific reports · 2025Article
- Therapeutic potential and pharmacological mechanisms of Traditional Chinese Medicine in gout treatment.Acta pharmacologica Sinica · 2025Review
- Lysosomal Stress in Cardiovascular Diseases: Therapeutic Potential of Cardiovascular Drugs and Future Directions.Biomedicines · 2025Review
- A New Perspective on the Prediction and Treatment of Stroke: The Role of Uric Acid.Neuroscience bulletin · 2025Review
- Uric acid reduces the expression of aquaporins in renal collecting ducts to increase urine output in hyperuricemia.Frontiers in physiology · 2025Article
- The prognostic significance of uric acid to albumin ratio in patients with aneurysmal subarachnoid hemorrhage following surgical clipping or endovascular interventions: insights from a large cohort study.Frontiers in neurology · 2025Article
- Uric Acid: A Biomarker and Pathogenic Factor of Affective Disorders and Neurodegenerative Diseases.Current pharmaceutical design · 2025Review
- Uric acid-induced cardiomyocytic polyamines' insufficience: a potential mechanism mediates cardiomyocytic injury.Frontiers in endocrinology · 2025Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Co-delivery of indomethacin and uricase as a new strategy for inflammatory diseases associated with high uric acid.Drug delivery and translational research · 2024Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uric acid crystal is known to activate the NLRP3 inflammasome and to cause tissue damages, which can result in many diseases, such as gout, chronic renal injury and myocardial damage. Meanwhile, soluble uric acid (sUA), before forming crystals, is also related to these diseases. This study was carried out to investigate whether sUA could also activate NLRP3 inflammasome in cardiomyocytes and to analyse the mechanisms. The cardiomyocyte activity was monitored, along with the levels of mature IL-1β and caspase-1 from H9c2 cells following sUA stimulus. We found that sUA was able to activate NLRP3 inflammasome, which was responsible for H9c2 cell apoptosis induced by sUA. By elevating TLR6 levels and then activating NF-κB/p65 signal pathway, sUA promoted NLRP3, pro-caspase 1 and pro-IL-1β production and provided the first signal of NLRP3 inflammasome activation. Meanwhile, ROS production regulated by UCP2 levels also contributed to NLRP3 inflammasome assembly and subsequent caspase 1 activation and mature IL-1β secretion. In addition, the tlr6 knockdown rats suffering from hyperuricemia showed the lower level of IL-1β and an ameliorative cardiac function. These findings suggest that sUA activates NLRP3 inflammasome in cardiomyocytes and they may provide one therapeutic strategy for myocardial damage induced by sUA.
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