Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease.
Abstract
Diabetic kidney disease (DKD) continues to pose a substantial public health challenge, in which cellular senescence is recognized as a pivotal driver of disease progression. While formononetin (FN) has been documented to exhibit anti-senescence properties, its potential as a therapeutic agent for DKD and the molecular mechanisms involved remain unexplored.
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Research summary
Formononetin inhibits the p53 signaling pathway to delay cellular senescence and ameliorate diabetic kidney disease. The paper addresses the role of cellular senescence in disease progression, which is a key factor in aging and longevity research.
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