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首页> 外文期刊>Immunology, endocrine & metabolic agents in medicinal chemistry. >The HGF/c-Met Receptor System Under Pathological Conditions
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The HGF/c-Met Receptor System Under Pathological Conditions

机译：病理条件下的HGF / c-Met受体系统

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Abstract: Hepatocyte growth factor (HGF) is a mesenchyme-derived pleiotropic factor which regulates cell growth, cell motility, and morphogenesis of various types of cells, and is thus considered a humoral mediator of morphogenic tissue interactions. Although HGF was originally identified as a potent mitogen for hepatocytes, it has also been identified as a member of angiogenic growth factors. Interestingly, the presence of its specific receptor, c-met, is observed not only in hepatocyte but also in vascular cells, cardiac myocytes, skeletal muscle, kidney cells, neuronal cell, and fibroblasts. On the other hand, vascular endothelial growth factor (VEGF) is also a growth factor for endothelial cells. The signal trans-duction of VEGF and HGF is quite similar in physiological condition, but differs in pathological condition. To investigate this difference between HGF and VEGF, we showed that HGF but not VEGF prevents the senescence EPC due to oxida-tive stress through the inhibition of racl. Moreover, we reported that HGF promotes SHIP-2 translocation from epithelial growth factor receptor (EGFR) to c-Met, and protects oxidative stress through EGFR degradation. By this anti-oxidative and anti-senescence effects of HGF would maintain the vessels long enough in patients receiving much oxidative stress. Another unique effect of HGF is anti-fibrosis. HGF does not inhibit TGF-(31 in physiological condition, but reduces it in pathological, we discuss the potential effect of condition by promoting the myofibroblast apoptosis, and inhibits the vicious cycle of TGF-beta1 and angiotensin II through the inhibition of PTEN activity.In this report HGF on pathological condition in cardiovascular diseases and chronic kidney disease (CKD).
机译：摘要：肝细胞生长因子（HGF）是间充质衍生的多效性因子，它调节细胞生长，细胞运动和各种类型细胞的形态发生，因此被认为是体液发生组织相互作用的体液介质。尽管最初将HGF鉴定为肝细胞的有效促分裂原，但也已将其鉴定为血管生成生长因子的成员。有趣的是，不仅在肝细胞中而且在血管细胞，心肌细胞，骨骼肌，肾细胞，神经元细胞和成纤维细胞中均观察到了其特异性受体c-met的存在。另一方面，血管内皮生长因子（VEGF）也是内皮细胞的生长因子。 VEGF和HGF的信号转导在生理条件下非常相似，但在病理条件上有所不同。为了研究HGF和VEGF之间的这种差异，我们发现HGF而非VEGF可以通过抑制racl来阻止由于氧化应激引起的衰老EPC。此外，我们报道了HGF促进SHIP-2从上皮生长因子受体（EGFR）转运至c-Met，并通过EGFR降解保护氧化应激。通过这种抗氧化和抗衰老的作用，HGF可以使接受大量氧化应激的患者的血管保持足够长的时间。 HGF的另一个独特作用是抗纤维化。 HGF在生理条件下不抑制TGF-（31），但在病理上降低其水平，我们讨论了通过促进成肌纤维细胞凋亡来缓解疾病的潜在作用，并通过抑制PTEN活性来抑制TGF-β1和血管紧张素II的恶性循环。在本报告中，HGF涉及心血管疾病和慢性肾脏病（CKD）的病理状况。

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