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

Acute myocardial infarction (AMI) is recognized to be a severe threat to people’s health conditions and life quality. The accumulation of hepatocyte growth factor (HGF) in ischemic myocardium has been observed in both processes of experimental ischemia and reperfusion (I/R) and permanent coronary ar...

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Detalles Bibliográficos
Autores principales: Zhang, Zaiyong, Long, Cheng, Guan, Yufeng, Song, Mingcai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PAGEPress Publications, Pavia, Italy 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445436/
https://www.ncbi.nlm.nih.gov/pubmed/32909423
http://dx.doi.org/10.4081/ejh.2020.3142
Descripción
Sumario:Acute myocardial infarction (AMI) is recognized to be a severe threat to people’s health conditions and life quality. The accumulation of hepatocyte growth factor (HGF) in ischemic myocardium has been observed in both processes of experimental ischemia and reperfusion (I/R) and permanent coronary artery occlusion. The aim of the study was to investigate the effect of HGF on myocardial cell apoptosis, ventricular remodeling and cardiac function after myocardial infarction (MI) in diabetic rats, and to explore whether the effect is mediated by HGF/c-Met signaling pathway. MI significantly increases LVWI and RVWI and myocardial apoptotic index, and up-regulates the expression of HGF and c-Met at mRNA and protein levels in MI control group. The LVWI and RVWI, and myocardial apoptosis were reduced by treatment with HGF, which also increased the myocardial cell viability and the expression of HGF and c-Met. In summary, HGF significantly attenuates myocardial apoptosis and improves cardiac function after AMI in diabetic rats by further enhancing the activation of HGF/c-Met pathway.