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Background <p>Acute myocardial infarction leads to myocardial inflammation and necroptosis, and is a major cause of heart failure, cardiovascular dysfunction, and mortality. Adverse remodeling and myocardial fibrosis following myocardial infarction are key pathophysiological processes contributing to poor prognosis. Licorice, a widely utilized herb and food, contains glabridin, a bioactive component that acts as a potent PPARγ agonist. Glabridin has demonstrated multiple beneficial biological effects, including antioxidative stress, anti-inflammation, anti-atherosclerosis, and tumor progression inhibition. However, its role in cardiovascular diseases remains understudied.</p> Methods <p>Using C57BL/6 mice, a myocardial infarction model was established <i>via</i> left coronary artery ligation. Mice were treated with glabridin by oral gavage daily for 4 consecutive weeks post-surgery. Cardiac function and various indicators were assessed to evaluate the therapeutic effects. Additionally, primary cardiac fibroblasts were isolated from the mice for in vitro experiments to verify the effects of glabridin and further explore its mechanism of action.</p> Results <p>Glabridin treatment significantly improved cardiac fibrosis and alleviated cardiac dysfunction in mice. Mechanistically, glabridin activates PPARγ, thereby promoting the ubiquitination and degradation of EGFR, inhibiting the activation of the downstream PI3K/Akt signaling pathway, and mitigating myocardial fibrosis progression.</p> Conclusion <p>Glabridin links the PI3K/Akt pathway and promote EGFR ubiquitination, offering insights into myocardial fibrosis mechanisms and potential therapeutic targets.</p> Graphical Abstract <p></p>

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Glabridin improves cardiac remodeling after myocardial infarction by activating PPARγ to regulate the ubiquitination and degradation of EGFR

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月21日

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  • Zixuan Li,
  • Yiran Hu,
  • Yu Jiang,
  • Bingqi Fu,
  • Tianxin Long,
  • Hao Huang,
  • Juwei Yang,
  • Min Gu,
  • Hongxia Niu,
  • Wei Hua

摘要

Background

Acute myocardial infarction leads to myocardial inflammation and necroptosis, and is a major cause of heart failure, cardiovascular dysfunction, and mortality. Adverse remodeling and myocardial fibrosis following myocardial infarction are key pathophysiological processes contributing to poor prognosis. Licorice, a widely utilized herb and food, contains glabridin, a bioactive component that acts as a potent PPARγ agonist. Glabridin has demonstrated multiple beneficial biological effects, including antioxidative stress, anti-inflammation, anti-atherosclerosis, and tumor progression inhibition. However, its role in cardiovascular diseases remains understudied.

Methods

Using C57BL/6 mice, a myocardial infarction model was established via left coronary artery ligation. Mice were treated with glabridin by oral gavage daily for 4 consecutive weeks post-surgery. Cardiac function and various indicators were assessed to evaluate the therapeutic effects. Additionally, primary cardiac fibroblasts were isolated from the mice for in vitro experiments to verify the effects of glabridin and further explore its mechanism of action.

Results

Glabridin treatment significantly improved cardiac fibrosis and alleviated cardiac dysfunction in mice. Mechanistically, glabridin activates PPARγ, thereby promoting the ubiquitination and degradation of EGFR, inhibiting the activation of the downstream PI3K/Akt signaling pathway, and mitigating myocardial fibrosis progression.

Conclusion

Glabridin links the PI3K/Akt pathway and promote EGFR ubiquitination, offering insights into myocardial fibrosis mechanisms and potential therapeutic targets.

Graphical Abstract