The guanine nucleotide exchange factor Rin-like is a repressor for renal uric acid excretion in human and mouse.

RINL acts as a repressor of renal uric acid excretion, with mutations increasing serum uric acid levels in humans and mice, highlighting its role in hyperuricemia.

• Why it matters: Understanding the molecular mechanisms behind uric acid regulation is crucial for developing targeted therapies for hyperuricemia, which affects about 14% of the population and can lead to gout and kidney disease.
• What they did: Researchers identified RINL as a regulator of uric acid excretion, discovered pathogenic mutations that increase RINL activity, and screened natural products, finding tetrahydrocurcumin that promotes RINL degradation to lower serum uric acid in mice.
• The result: Targeting RINL degradation effectively reduces hyperuricemia in mouse models, suggesting that RINL inhibition could be a promising therapeutic approach for managing hyperuricemia in humans.