ArticleCells2022
Asymptomatic Hyperuricemia Promotes Recovery from Ischemic Organ Injury by Modulating the Phenotype of Macrophages.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- Mild Hyperuricemia Attenuates Salt-Sensitive Hypertension and Kidney Damage.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Genome analysis of a newly isolated Lysinibacillus fusiformis-YC01 for biodegrading inosine and guanosine.Biodegradation · 2025Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Interaction between anemia and hyperuricemia in the risk of all-cause mortality in patients with chronic kidney disease.Frontiers in endocrinology · 2024Article
- Transcutaneous measurement of renal function in two rodent models of obstructive nephropathy.BMC research notes · 2023Article
- Asymptomatic hyperuricaemia in chronic kidney disease: mechanisms and clinical implications.Clinical kidney journal · 2023Review
- Uric Acid and Chronic Kidney Disease: Still More to Do.Kidney international reports · 2023Review
- The dysregulation of immune cells induced by uric acid: mechanisms of inflammation associated with hyperuricemia and its complications.Frontiers in immunology · 2023Review
- Nrf2 Activation in Chronic Kidney Disease: Promises and Pitfalls.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Acute organ injury, such as acute kidney injury (AKI) and disease (AKD), are major causes of morbidity and mortality worldwide. Hyperuricemia (HU) is common in patients with impaired kidney function but the impact of asymptomatic HU on the different phases of AKI/AKD is incompletely understood. We hypothesized that asymptomatic HU would attenuate AKD because soluble, in contrast to crystalline, uric acid (sUA) can attenuate sterile inflammation. In vitro, 10 mg/dL sUA decreased reactive oxygen species and interleukin-6 production in macrophages, while enhancing fatty acid oxidation as compared with a physiological concentration of 5 mg/dL sUA or medium. In transgenic mice, asymptomatic HU of 7-10 mg/dL did not affect post-ischemic AKI/AKD but accelerated the recovery of kidney excretory function on day 14. Improved functional outcome was associated with better tubular integrity, less peritubular inflammation, and interstitial fibrosis. Mechanistic studies suggested that HU shifted macrophage polarization towards an anti-inflammatory M2-like phenotype characterized by expression of anti-oxidative and metabolic genes as compared with post-ischemic AKI-chronic kidney disease transition in mice without HU. Our data imply that asymptomatic HU acts as anti-oxidant on macrophages and tubular epithelial cells, which endorses the recovery of kidney function and structure upon AKI.
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Registered trials
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