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Updated: Jun 3, 2025
Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
Published on: November 28, 2015
Tigulixostat Alleviates Hyperuricemic Nephropathy by Promoting M2 Macrophage Polarization
Lina Xue1,2, Qianru Tao1,2, Haining Chang1
1Department of Internal Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People's Republic of China.
Purpose:
Serum uric acid (SUA) is primarily produced through the hydrolysis of purines in the liver, with its excretion largely handled by the kidneys. Urate transporter 1 (URAT1) inhibitors are known to enhance uric acid elimination via the kidneys, but they also increase the risk of kidney stone formation. Currently, xanthine oxidase (XO) inhibitors are the predominant uric-lowering medications on the market.
Methods:
In this study, we utilized single-cell RNA sequencing, spatial metabolomics, plasma metabolomics, flow cytometry to explore the effects of Tigulixostat on uric acid level and hyperuricemic nephropathy (HN) in Uox-KO mouse model.
Results:
In this study, we discovered that Tigulixostat (LC350189) more effectively reduced SUA levels and resulted in better renal outcomes compared to allopurinol, without inducing liver injury in urate oxidase knockout (Uox-KO) mice. Mechanistically, we found that Tigulixostat improved HN by promoting M2 macrophage polarization.
Conclusion:
These findings suggest Tigulixostat as a promising therapeutic option for managing hyperuricemia and related kidney conditions.
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