Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

Key Points

• Formononetin significantly delays cellular senescence, offering therapeutic benefits against diabetic kidney disease.
• In both cellular and animal models, formononetin effectively suppresses the p53 signaling pathway by an unspecified mechanism.
• The findings show a clear link between p53 signaling and cellular aging, with implications for kidney disease treatment.
• These results underscore the need for further studies to explore formononetin's potential in clinical applications.

Abstract