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肾纤维化即肾小球和肾小管瘢痕形成,是所有形式的肾脏慢性衰竭的最终转归,寻找这个过程中重要的影响因素,并通过改变这些因素进而终止整个纤维化进程是目前尚未解决的医学难题。KCa 3.1在肾纤维母细胞增殖和纤维化进展过程中扮演着重要角色;血管紧张素Ⅱ可同时刺激转化生长因子-β(TGF-β)和表皮生长因子受体(EGFR),EG-FR是TGF-β介导的肾脏纤维化过程的上游信号物质;Toll样受体-4可以减轻肾小管损害,能够通过改变肾脏细胞对TGF-β的敏感性促进肾纤维化,也是启动TGF-β促进纤维化的关键物质,肥大细胞在整个纤维化过程中体现出促进和延缓两种截然不同的功能。
Renal fibrosis, glomerular and tubular scarring, is the ultimate outcome of all forms of chronic kidney failure. Finding an important factor in this process and ending the entire fibrosis process by changing these factors is currently unsolved Medical problems. KCa 3.1 plays an important role in the progression of renal fibroblasts proliferation and fibrosis; Angiotensin II can simultaneously stimulate the expression of transforming growth factor-β (TGF-β) and epidermal growth factor receptor (EGFR), and EG-FR is TGF-β-mediated renal fibrosis upstream signal substance; Toll-like receptor-4 can reduce tubular damage, by changing the sensitivity of renal cells to TGF-β promote renal fibrosis, but also to promote TGF-β promote The key substance of fibrosis, mast cells in the entire process of fibrosis to promote and delay two distinct functions.