IJCEMR
Research Progress on the Mechanism of Kidney Injury Associated with Hyperuricemia
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Abstract
Hyperuricemia (HUA) has become one of the global public health problems, and the mechanisms of renal injury caused by it have received increasing attention. This review focuses on the main mechanisms of hyperuricemia-associated renal injury, including the effects of three aspects: monosodium urate (MSU) crystal deposition, activated NLRP3 inflammasome, and mito-chondrial dysfunction. We explored in detail how MSU crystals lead to kidney injury by inducing oxidative stress, inflammatory responses, and apoptosis. Second, we found that the activation of NLRP3 inflammatory vesicles plays a key role in hyperuricemia-induced renal injury by triggering a strong inflammatory response and further destroying renal tissues. Finally, we also discussed the importance of mitochondrial dysfunction in hyperuricemia-induced kidney injury, noting that mitochondrial dysfunction may exacerbate kidney injury by affecting cellular energy metabolism and modulating cell death pathways. Through a comprehensive understanding of these mechanisms, we hope to provide new ideas for the prevention and treatment of hyperuricemia-associated kidney disease.
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How to cite this paper
Research Progress on the Mechanism of Kidney Injury Associated with Hyperuricemia
How to cite this paper: Jianchun Chen, Xiaoying Yang, Caizhong Zhang, Wanping Lv. (2024) Research Progress on the Mechanism of Kidney Injury Associated with Hyperuricemia. International Journal of Clinical and Experimental Medicine Research, 8(1), 187-190.
DOI: http://dx.doi.org/10.26855/ijcemr.2024.01.032
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