The mechanism of hypoxia-inducible factor-1α in gouty nephropathy

Gouty nephropathy (GN) comprises a group of renal injuries caused by monosodium urate (MSU) deposition in the kidneys under conditions of long-term hyperuricemia (HUA), and its incidence has continued to rise each year. In the pathological process of GN, hypoxia-inducible factor-1α (HIF-1α) participates in the regulation of inflammation, oxidative stress, and renal interstitial fibrosis, showing dual influences on disease development. Therefore, the regulation of HIF-1α is considered one of the major strategies for GN treatment. Current therapeutic approaches involve direct suppression of its activity as well as indirect modulation. HIF stabilizers and related agents have displayed therapeutic potential for GN in animal experiments. Further clarification of the complicated mechanisms of HIF-1α during the pathological progression of GN may offer new ideas and potential targets for preventing and treating this disease.