自体动静脉内瘘(arteriovenous fistula,AVF)是血液透析(hemodialysis,HD)患者首选的血管通路，也是终末期肾病(end-stage renal disease,ESRD)患者维持生命的重要渠道。AVF功能障碍增加了ESRD患者住院率及死亡率。目前AVF功能障碍发生机制尚未明确，但其常见原因有血管重塑不足、新生内膜增生(neointimal hyperplasia,NIH)导致的非血栓性血管狭窄。作为Toll样受体(toll- like receptors,TLRs)重要成员的TLR4，在介导血管平滑肌细胞(vascular smooth muscle cells,VSMCs)等细胞的增殖、迁移及细胞外基质(extracellular matrix,ECM)沉积所诱发的NIH致血管狭窄的病理进程中具有关键作用。了解TLR4在AVF狭窄中的确切机制是解决AVF远期通畅问题的当务之急。本文将从AVF狭窄及影响因素、TLR4概述及TLR4/核因子κB(nuclear factor kappa B,NF-κB)信号通路对AVF狭窄的调控作用进行综述。

Autologous arteriovenous fistula (AVF) is the preferable vascular access method for hemodialysis (HD), being a critical route for end-stage renal disease (ESRD) patients to maintain their lives. AVF dysfunction increases the hospitalization rate and mortality of ESRD patients. The mechanism of AVF dysfunction has not been fully elucidated, but insufficient vascular remodeling and neointimal hyperplasia have been considered as the main causes of non-thrombotic vascular stenosis. Toll-like receptor 4 (TLR4), an important member in the toll-like receptor family, mediates the proliferation and migration of vascular smooth muscle cells (VSMCs) and deposition of extracellular matrix in AVF wall, leading to intimal hyperplasia and AVF stenosis. Comprehension of TLR4 in the development of AVF dysfunction is closely related to the accurate diagnosis and treatment of AVF dysfunction and maintenance of long-term patency of AVF. Here we summarize the recent progresses in AVF stenosis, its influencing factors, TLR4, and the role of TLR4/NF-κB signal pathway in the pathogenesis of AVF dysfunction.