Department of Nephrology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Front Med. 2017 Sep;11(3):349-358. doi: 10.1007/s11684-017-0571-2. Epub 2017 Aug 8.
Peritoneal dialysis (PD) is an established form of renal replacement therapy. Long-term PD leads to morphologic and functional changes to the peritoneal membrane (PM), which is defined as peritoneal fibrosis, a known cause of loss of peritoneal ultrafiltration capacity. Inflammation and angiogenesis are key events during the pathogenesis of peritoneal fibrosis. This review discusses the pathophysiology of peritoneal fibrosis and recent research progress on key fibrogenic molecular mechanisms in peritoneal inflammation and angiogenesis, including Toll-like receptor ligand-mediated, NOD-like receptor protein 3/interleukin-1β, vascular endothelial growth factor, and angiopoietin-2/Tie2 signaling pathways. Furthermore, novel strategies targeting peritoneal inflammation and angiogenesis to preserve the PM are discussed in depth.
腹膜透析(PD)是一种已确立的肾脏替代治疗形式。长期 PD 会导致腹膜(PM)的形态和功能发生变化,这被定义为腹膜纤维化,是导致腹膜超滤能力丧失的已知原因。炎症和血管生成是腹膜纤维化发病机制中的关键事件。本文讨论了腹膜纤维化的病理生理学以及腹膜炎症和血管生成中关键纤维化分子机制的最新研究进展,包括 Toll 样受体配体介导的、NOD 样受体蛋白 3/白细胞介素-1β、血管内皮生长因子和血管生成素-2/Tie2 信号通路。此外,还深入讨论了针对腹膜炎症和血管生成以保护 PM 的新策略。