Hepatocyte growth factor (HGF) is released by stressed human vascular cells and promotes vascular cell repair responses in both autocrine and paracrine ways. Subjects with a low capacity to express HGF in response to systemic stress have an increased cardiovascular risk. Human atherosclerotic plaques with a low content of HGF have a more unstable phenotype. The present study shows that subjects with a low ability to express HGF in response to metabolic stress have an increased risk to suffer myocardial infarction and stroke.
Keywords: AU, arbitrary unit; BrdU, bromodeoxyuridine; CVD, cardiovascular disease; EC, endothelial cell; HCASMC, human coronary artery smooth muscle cell; HDL, high-density lipoprotein; HGF, hepatocyte growth factor; HUVEC, human umbilical cord endothelial cell; ICD-9, International Classification of Diseases-9th Revision; IL, interleukin; LDL, low-density lipoprotein; MMP, matrix metalloproteinase; PlGF, placental growth factor; SMC, smooth muscle cell; TGF, transforming growth factor; TNF, tumor necrosis factor; TRAIL, tumor necrosis factor–related apoptosis-inducing ligand; VEGF, vascular endothelial growth factor; apoptosis; atherosclerosis; endothelial cells; growth factors; injury; mRNA, messenger RNA; myocardial infarction; s, soluble; si-HGF, hepatocyte growth factor small interfering RNA; siRNA, small interfering RNA.
© 2022 The Authors.