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Background/Objective: Arteriovenous fistulas (AVFs) are the preferred vascular access for hemodialysis of patients with end-stage renal disease. However, there is a high incidence of AVF failures caused by insufficient outward remodeling or venous neo-intimal hyperplasia formation. Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play an important role in many cardiovascular diseases. Abnormal VSMC proliferation and migration could be abolished by inhibition of mitochondrial division. Method: We found that abnormal proliferation and migration of VSMCs and increased mitochondrial fission were associated with AVF stenosis in patients. We also investigated the mechanisms, particularly the role of mitochondrial dynamics, underlying these VSMC behaviors. In vitro, we observed that inhibition of mitochondrial fission and Akt phosphorylation can diminish proliferation and migration of VSMCs induced by platelet-derived growth factor-BB (PDGF-BB). In vivo, daily intraperitoneal injections of mitochondrial division inhibitor 1 (Mdivi-1) decreased VSMC proliferation and reduced AVF wall thickness in a rat AVF model. Conclusion and Result: Our results suggest that inhibition of mitochondrial fission improves AVF patency by reducing wall thickening through the PI3K/Akt signaling pathway. Therefore, inhibition of mitochondrial fission has the clinical potential to improve AVF patency. [ABSTRACT FROM AUTHOR]

Epigenetic changes, particularly non‐coding RNAs, have been implicated extensively in the pathogenesis of vascular diseases. Specific miRNAs are involved in the differentiation, phenotypic switch, proliferation, apoptosis, cytokine production and matrix deposition of endothelial cells and/or vascular smooth muscle cells. MicroRNA‐125b has been studied in depth for its role in carcinogenesis with a double‐edged role; that is, it can act as an oncogene in some cancer types and as a tumour suppressor gene in others. However, cumulative evidence from the use of advanced miRNA profiling techniques and bioinformatics analysis suggests that miR‐125b can be a potential mediator and useful marker of vascular diseases. Currently, the exact role of miR‐125b in vascular diseases is not known. In this systematic review, we intend to provide an updated compilation of all the recent findings of miR‐125b in vascular diseases, using a systematic approach of retrieving data from all available reports followed by data summarization. MiR‐125b serves as a pathogenic player in multiple vascular pathologies involving endothelia and vascular smooth muscle cells and also serves as a diagnostic marker for vascular diseases. We further provide a computational biologic presentation of the complex network of miR‐125b and its target genes within the scope of vascular diseases. [ABSTRACT FROM AUTHOR]

Abstract: Percutaneous transluminal coronary angioplasty (PTCA) was developed as a nonsurgical alternative to coronary artery bypass graft surgery (CABG). Its limitations led to the introduction of stents. The introduction of baremetal stents (EMS) virtually eliminated the acute complications of PTCA. Drug-eluting stents (DES) were developed to combat the neo-intimal hyperplasia; and a marked reduction in restenosis rate and target lesion revascularization (TLR) was obtained with their use as compared to BMS. [Copyright &y& Elsevier]

In-stent restenosis reflects the interaction of a cascade of molecular and cellular events occurring within the vessel wall. Coronary stenting induces localized injury to the vessel wall, which leads to the release of thrombogenic, vasoactive, and lymphocytes mitogenic factors that result in processes causing re-narrowing at the injured site. Three major processes have been identified that lead to the in-stent restenosis: neointimal hyperplasia, elastic recoil, and negative arterial remodeling. The most important one is intimal hyperplasia. As the time course of neointimal hyperplasia is unknown, a causal relationship between the development of new blood vessels and clinical restenosis cannot be firmly established. [ABSTRACT FROM AUTHOR]

End-to-end autogenous vein-to-artery grafts in rats have been used extensively as a model for neointimal thickening (hyperplasia), which develops over the first 6 weeks after grafting. This study employed computerised morphometric techniques to analyse 16 grafts, in order to quantitate precisely how the neointima develops. Two important features were described that have not been identified previously, due to the extensive variation in neo-intimal thickness inherent in vein grafts. Firstly, the proximal region of the graft was significantly thicker than the distal region, up until 6 months after grafting. The smooth muscle cells in the graft may have developed more rapidly in the proximal region, due to the altered haemodynamics within the graft. Secondly, within the central region of the graft the characteristic focal nature of neo-intimal hyperplasia was evident throughout the period of the study, but by 6 months the neo-intima tended to be distrubuted more evenly. By 6 months remodelling of smooth muscle throughout the graft neo-intima had occurred, and the neo-intima had matured to a thickness equivalent to that of the intima plus media of the adjacent iliac artery. [ABSTRACT FROM AUTHOR]

Introduction:: Arteriovenous fistula is the best choice for vascular access in hemodialysis patients. However, arteriovenous fistula dysfunction is a major clinical issue. The most common cause of arteriovenous fistula failure is intimal hyperplasia. In this study, we have investigated the effect of N-acetylcysteine on neo-intimal hyperplasia after arteriovenous fistula creation in rats., Methods:: This study was conducted in 24 rats which were randomly divided into two groups: control and N-acetylcysteine groups. An end-to-side anastomosis was made between the femoral artery and vein. The control group received distilled water intraperitoneally while the animals in N-acetylcysteine group received 300 mg/kg/day of N-acetylcysteine via the same route. After 28 days, the thickness of intima and media was measured using hematoxylin and eosin., Results:: There was no significant difference between the two groups regarding age ( p = 0.6) and weight ( p = 0.1). The mean intima thickness in N-acetylcysteine group was significantly less than control group (17 ± 20 and 119 ± 46 µm, respectively; p < 0.001). The mean intima/media thickness in the N-acetylcysteine group was significantly less than control group (0.5 ± 0.63 vs 2.05 ± 1.17 µm; p < 0.001)., Conclusion:: N-acetylcysteine is effective in inhibiting neo-intimal hyperplasia in a rat model of arteriovenous fistula.