The anatomical sources of neointimal cells in the arteriovenous fistula

Abstract

Neointimal cells are an elusive population with ambiguous origins, functions, and states of differentiation. Expansion of the venous intima in arteriovenous fistula (AVF) is one of the most prominent remodeling processes in the wall after access creation. However, most of the current knowledge about neointimal cells in AVFs comes from extrapolations from the arterial neointima in non-AVF systems. Understanding the origin of neointimal cells in fistulas may have important implications for the design and effective delivery of therapies aimed to decrease intimal hyperplasia (IH). In addition, a broader knowledge of cellular dynamics during postoperative remodeling of the AVF may help clarify other transformation processes in the wall that combined with IH determine the successful remodeling or failure of the access. In this review, we discuss the possible anatomical sources of neointimal cells in AVFs and their relative contribution to intimal expansion.

Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure

“…The artery injury model is induced by completely removing the endothelial layer and causing a distending mural injury in rat/mice with normal kidney function (48). In patients with kidney failure, uremic milieu contributes to a multitude of vascular diseases including venous intimal hyperplasia even prior to hemodialysis access surgery (7,49,50). Our studies showed that expression level of endothelial JMJD3 in vessel was significantly decreased in the context of chronic renal failure.…”

“…Neointimal hyperplasia (NIH) is present in most native veins and AVFs, which is prominent in many patients with kidney failure (7). After AVF creation, expansion of neointima may aggravate inward remodeling leading to the development of stenosis and access failure.…”

Effect of exercises on the maturation of newly created arteriovenous fistulas over distal and proximal upper limb: A systematic review and meta-analysis

“…This in turn may lead to neointimal hyperplasia and venous stenosis. 24,25 Muscle contractions occurring during upper limb exercise training is the major stimulus to increase blood flow and WSS. 26 It has been found to be associated with endothelium-dependent vasodilation, probably through an increase in nitric oxide (NO) bioactivity.…”

The Potential Roles of CHI3L1 in Failed Autologous Arteriovenous Fistula in End-Stage Renal Disease

“…Stenosis can be located in any part of the vascular access, but it is most common at the venous end and the anastomosis of the internal fistula. The main pathological basis is venous intima hyperplasia (Vazquez-Padron et al 2021), which is composed of endothelial cells, vascular smooth muscle cells (SMCs), macrophages, fibroblasts, myofibroblasts and a large amount of extracellular matrix (ECM), while CHI3L1 is expressed by different types of cells including SMCs, macrophages, neutrophils (Yeo et al 2019). Thus, it is supposed that CHI3L1 might also have an impact on the failure of AVF in ESRD patients, apart from the molecular mechanisms already demonstrated by several studies, such as inflammation, uremia, hypoxia, and sheer stress, which are responsible for the AVF failure (Brahmbhatt et al 2016).…”