Hepatocyte growth factor intervention to reduce myocardial injury and improve cardiac function on diabetic myocardial

Zaiyong Zhang1, Cheng Long2, Yufeng Guan3

  • 1Department of Cardiology, Panyu Central Hospital; Cardiovascular Institute of Panyu District; School of Life Sciences, South China Normal University, Guangzhou. Dr_zaiyong@126.com.

Insights

Hepatocyte growth factor (HGF) treatment reduced heart cell apoptosis and improved cardiac function in diabetic rats with myocardial infarction. This effect was mediated by the HGF/c-Met signaling pathway.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Diabetology

Background:

  • Acute myocardial infarction (AMI) poses a significant threat to health and quality of life.
  • Hepatocyte growth factor (HGF) accumulates in ischemic myocardium during experimental ischemia/reperfusion and permanent coronary artery occlusion.
  • The role of HGF in diabetic myocardial infarction requires further investigation.

Purpose of the Study:

  • To investigate the effect of HGF on myocardial apoptosis, ventricular remodeling, and cardiac function in diabetic rats after myocardial infarction (MI).
  • To explore the involvement of the HGF/c-Met signaling pathway in mediating these effects.

Main Methods:

  • Induction of myocardial infarction in diabetic rat models.
  • Administration of HGF to assess its impact on cardiac parameters.
  • Measurement of left ventricular (LVWI) and right ventricular (RVWI) work indices, myocardial apoptotic index, and expression of HGF and c-Met at mRNA and protein levels.

Main Results:

  • Myocardial infarction significantly increased LVWI, RVWI, and myocardial apoptosis, while up-regulating HGF and c-Met expression.
  • HGF treatment reduced LVWI, RVWI, and myocardial apoptosis in MI rats.
  • HGF administration enhanced myocardial cell viability and increased the expression of HGF and c-Met.

Conclusions:

  • HGF significantly attenuates myocardial apoptosis after AMI in diabetic rats.
  • HGF treatment improves cardiac function in diabetic rats with myocardial infarction.
  • The beneficial effects of HGF are mediated by enhancing the activation of the HGF/c-Met signaling pathway.

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