We examined a coronary artery disease predictive algorithm (CADPA) that includes 9 biomarkers involved in the pathogenesis of atherosclerosis initiated by endothelial damage and repair (hepatocyte growth factor, soluble FAS, Fas ligand, eotaxin, cutaneous T cell-attracting chemokine, monocyte chemotactic protein-3, interleukin-16, hemoglobin A1c, high-density lipoprotein-cholesterol), in addition to age, gender, diabetes, and family history of myocardial infarction that more accurately predicts 5-year risk of ACS to identify the patient population at discordantly high risk.
Serum hepatocyte growth factor (HGF) is positively associated with poor prognosis of heart failure and myocardial infarction, and it can also predict the risk of ischemic stroke in population.
However, recent studies suggested that angiogenic growth factors have pleiotropic effects that may contribute to outcome so we expanded focus of our work to investigate potential mechanisms underlying action of VEGF165, HGF and their combination in MI.
The present study evaluated the therapeutic effects of hepatocyte growth factor (HGF) gene-engineered skeletal myoblasts on tissue regeneration and restoration of heart function in a rat MI model.
We tested a novel small-molecular hydrogel (SMH) on whether it could provide a scaffold for hepatocyte growth factor (HGF)-modified MSCs and alleviate ventricular remodeling while preserving cardiac function after MI.
Cardiac-specific expression of the hepatocyte growth factor (HGF) under the control of a TnIc promoter confers a heart protective effect after myocardial infarction (MI).
The seeded scaffolds were transplanted in rats two weeks after MI (group: PU-HGF-SkM) or the infection solution was intramyocardially injected (group: Inj-HGF-SkM).
In conclusion, EPO accelerates angiogenesis via the upregulation of systemic levels such as HGF and FGF, and the local expression of VEGF and IGF, in porcine MI.
Mesenchymal stem cells modified with stromal cell-derived factor 1 alpha improve cardiac remodeling via paracrine activation of hepatocyte growth factor in a rat model of myocardial infarction.
1.There is growing evidence of the beneficial effects of hepatocyte growth factor (HGF) in myocardial infarction, heart failure and occlusive peripheral arterial disease.
Four weeks after MI, rats were randomly divided into a control group (n=11), HGF group (Adenovirus vector carrying human HGF (Ad-HGF)-transfected MSC transplanted into the infarct zone; n=11), G-CSF group (intraperitoneal injection with G-CSF; n=11), and HGF + G-CSF group (Ad-HGF-transfected MSC transplanted into the infarct zone and intraperitoneal injection with G-CSF; n=11).
Hepatocyte growth factor (HGF) reportedly exerts beneficial effects on the heart following myocardial infarction and during nonischemic cardiomyopathy, but the precise mechanisms underlying the latter have not been well elucidated.
Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium.
Four weeks after myocardial infarction (MI), Sprague Dawley rats were randomly divided into saline control group, MSC-GFP group, MSC-HGF group, and MSC-HGF+CsA group.
Based on these facts, we hypothesized that HGF may prevent restenosis after angioplasty through re endothelialization and myocardial infarction through induction of angiogenesis.