1. Academic Validation
  2. Diosgenin improves post-myocardial infarction cardiac function via HAND2-induced angiogenesis

Diosgenin improves post-myocardial infarction cardiac function via HAND2-induced angiogenesis

  • Biochem Biophys Res Commun. 2024 Jun 18:712-713:149941. doi: 10.1016/j.bbrc.2024.149941.
Xuehua Liu 1 Dehong Shen 2 Longfei Liu 2 Yuzhu Peng 3 Qiulun Lu 4
Affiliations

Affiliations

  • 1 Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, 210008, China; Cardiac Department, Sir Runrun Hospital Affiliated to Nanjing Medical University, Nanjing, 211166, China.
  • 2 Key Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, China.
  • 3 Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, 210008, China. Electronic address: pyz1131@163.com.
  • 4 Key Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, China. Electronic address: qiulunlu@njmu.edu.cn.
Abstract

While diosgenin has been demonstrated effective in various cardiovascular diseases, its specific impact on treating heart attacks remains unclear. Our research revealed that diosgenin significantly improved cardiac function in a myocardial infarction (MI) mouse model, reducing cardiac fibrosis and cell Apoptosis while promoting angiogenesis. Mechanistically, diosgenin upregulated the Hand2 expression, promoting the proliferation and migration of endothelial cells under hypoxic conditions. Acting as a transcription factor, HAND2 activated the angiogenesis-related gene Aggf1. Conversely, silencing Hand2 inhibited the diosgenin-induced migration of hypoxic endothelial cells and angiogenesis. In summary, these findings provide new insights into the protective role of diosgenin in MI, validating its effect on angiogenic activity and providing a theoretical basis for clinical treatment strategies.

Keywords

Angiogenesis; Diosgenin; HAND2; Myocardial infarction.

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