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

Our findings demonstrate that FN confers significant therapeutic benefits against DKD in both cellular and animal models. The mechanism underlying these benefits involves the delay of cellular senescence through suppression of the p53 signaling pathway.

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

Key Points

Abstract

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