Matsumoto K, Nakamura T
Division of Biochemistry, Biomedical Research Center, Osaka University Graduate School of Medicine, Osaka, Japan.
Kidney Int. 2001 Jun;59(6):2023-38. doi: 10.1046/j.1523-1755.2001.00717.x.
Hepatocyte growth factor (HGF), a ligand for the c-Met receptor tyrosine kinase, has mitogenic, motogenic, anti-apoptotic, and morphogenic (for example, induction of branching tubulogenesis) activities for renal tubular cells, while it has angiogenic and angioprotective actions for endothelial cells. Stromal cells such as mesangial cells, endothelial cells, and macrophages are sources of renal HGF; thus, HGF mediates epithelial-stromal and endothelial-mesangial interactions in the kidney. In response to acute renal injury, the expression of HGF increases in the injured kidney and in distant intact organs such as the lung and spleen. Locally and systemically increased HGF supports renal regeneration, possibly not only by enhancing cell growth but also by promoting morphogenesis of renal tissue. During progression of chronic renal failure/renal fibrosis, the expression of HGF decreases in a manner reciprocal to the increase in expression of transforming growth factor-beta (TGF-beta), a key player in tissue fibrosis. A decrease in endogenous HGF, as well as increase in TGF-beta, augments susceptibility to the onset of chronic renal failure/renal fibrosis. On the other hand, supplements of exogenous HGF have preventive and therapeutic effects in cases of acute and chronic renal failure/renal fibrosis in laboratory animals. HGF prevents epithelial cell death and enhances regeneration and remodeling of renal tissue with injury or fibrosis. A renotropic system underlies the vital potential of the kidney to regenerate, while an impaired renotropic system may confer susceptibility to the onset of renal diseases. Thus, HGF supplementation may be one therapeutic strategy to treat subjects with renal diseases, as it enhances the intrinsic ability of the kidney to regenerate.
肝细胞生长因子(HGF)是c-Met受体酪氨酸激酶的配体,对肾小管细胞具有促有丝分裂、促运动、抗凋亡和形态发生(例如诱导分支小管形成)活性,而对内皮细胞具有血管生成和血管保护作用。系膜细胞、内皮细胞和巨噬细胞等基质细胞是肾脏HGF的来源;因此,HGF介导肾脏中的上皮-基质和内皮-系膜相互作用。在急性肾损伤时,HGF在受损肾脏以及肺和脾等远处完整器官中的表达增加。局部和全身HGF增加不仅可能通过促进细胞生长,还通过促进肾组织的形态发生来支持肾脏再生。在慢性肾衰竭/肾纤维化进展过程中,HGF的表达以与组织纤维化关键因子转化生长因子-β(TGF-β)表达增加相反的方式降低。内源性HGF减少以及TGF-β增加会增加慢性肾衰竭/肾纤维化发病的易感性。另一方面,补充外源性HGF对实验动物的急性和慢性肾衰竭/肾纤维化具有预防和治疗作用。HGF可防止上皮细胞死亡,并增强损伤或纤维化肾组织的再生和重塑。促肾系统是肾脏再生重要潜能的基础,而受损的促肾系统可能会增加患肾病的易感性。因此,补充HGF可能是治疗肾病患者的一种治疗策略,因为它增强了肾脏的内在再生能力。