“Venopathy” at work: recasting neointimal hyperplasia in a new light

Hemodialysis vascular access is a unique form of vascular anastomosis. Although it is created in a unique disease state, it has much to offer in terms of insights into venous endothelial and anastomotic biology. The development of neointimal hyperplasia (NH) has been identified as a pathologic entity, decreasing the lifespan and effectiveness of hemodialysis vascular access. Subtle hints and new data suggest a contrary idea—that NH, to some extent an expected response, if controlled properly, may play a beneficial role in the promotion of maturation to a functional access. This review attempts to recast our understanding of NH and redefine research goals for an evolving discipline that focuses on a life-sustaining connection between an artery and vein.

Abbreviations: ACE, angiotensin-converting enzyme, AVF, arteriovenous fistulae, AVG, arteriovenous graft, BMP-7, Bone morphogenic protein-7, CD40L, CD40 ligand, End-MT, endothelial-mesenchymal transition, Hcy, homocysteine, HO-1, heme oxygenase 1, IEL, internal elastic lamina, IL, interleukin, IVUS, intravascular ultrasound, MMP, metalloproteinase, NH, neointimal hyperplasia, PAI-1, plasminogen activator inhibitor-1, PLGA, (Ptx)-loaded poly(lactic-co-glycolic acid), PTFE, polytetrafluoroethylene, ROCK, Rho kinase, SMC, smooth muscle cell, SNP, Single nucleotide polymorphisms’, TGF-β, transforming growth factor-β, VCAM-1, vascular cellular adhesion molecule-1