Xiao Yuxuan, Vazquez-Padron Roberto I, Martinez Laisel, Singer Harold A, Woltmann Daniel, Salman Loay H
Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, USA.
DeWitt Daughtry Family Department of Surgery, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, USA.
J Vasc Access. 2024 Mar;25(2):390-406. doi: 10.1177/11297298221085458. Epub 2022 Jun 24.
The rate of arteriovenous fistula (AVF) maturation failure remains unacceptably high despite continuous efforts on technique improvement and careful pre-surgery planning. In fact, half of all newly created AVFs are unable to be used for hemodialysis (HD) without a salvage procedure. While vascular stenosis in the venous limb of the access is the culprit, the underlying factors leading to vascular narrowing and AVF maturation failure are yet to be determined. We have recently demonstrated that AVF non-maturation is associated with post-operative medial fibrosis and fibrotic stenosis, and post-operative intimal hyperplasia (IH) exacerbates the situation. Multiple pathological processes and signaling pathways are underlying the stenotic remodeling of the AVF. Our group has recently indicated that a pro-inflammatory cytokine platelet factor 4 (PF4/CXCL4) is upregulated in veins that fail to mature after AVF creation. Platelet factor 4 is a fibrosis marker and can be detected in vascular stenosis tissue, suggesting that it may contribute to AVF maturation failure through stimulation of fibrosis and development of fibrotic stenosis. Here, we present an overview of the how PF4-mediated fibrosis determines AVF maturation failure.
尽管在技术改进和术前精心规划方面不断努力,但动静脉内瘘(AVF)成熟失败率仍然高得令人无法接受。事实上,所有新创建的AVF中有一半在没有补救措施的情况下无法用于血液透析(HD)。虽然通路静脉端的血管狭窄是罪魁祸首,但导致血管狭窄和AVF成熟失败的潜在因素尚未确定。我们最近证明,AVF未成熟与术后内侧纤维化和纤维化狭窄有关,术后内膜增生(IH)会使情况恶化。多种病理过程和信号通路是AVF狭窄重塑的基础。我们小组最近指出,促炎细胞因子血小板因子4(PF4/CXCL4)在AVF创建后未能成熟的静脉中上调。血小板因子4是一种纤维化标志物,可在血管狭窄组织中检测到,这表明它可能通过刺激纤维化和纤维化狭窄的发展导致AVF成熟失败。在此,我们概述PF4介导的纤维化如何决定AVF成熟失败。