Angioscopy in Transluminal Balloon and Laser Angioplasty in the Management of Chronic Hemodialysis Fistulae

Koga, Nobuhiko; Sato, Takashi; Baba, Tomomi T.; Ueda, Osamu; Okazaki, Hidetaka; Kohchi, Kyoji; Norita, Hiroaki; Maw, Paul R.; Moriyama, Atsuo

doi:10.1097/00002480-198907000-00005

Cited by 6 publications

(7 citation statements)

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“…For the size of intimal injury that resulted from the hemodialysis needle puncture, endothelial cells require 7–8 days to repopulate 3 . This explains that the medial layer of AVF can be visualized upon angioscopic examination 2 . In our 7‐day high phosphate treatment experiment, we observed that venous SMCs underwent osteogenic transdifferentiation in a time‐dependent manner (Figure S3).…”

Section: Discussionmentioning

confidence: 77%

“…3 This explains that the medial layer of AVF can be visualized upon angioscopic examination. 2 In our 7-day high phosphate treatment experiment, we observed that venous SMCs underwent osteogenic transdifferentiation in a time-dependent manner (Figure S3). Although we adopt the 3-day high-phosphate protocol (the chemical cue) to accentuate the synergistic effect from the physical cue, we could expect that the calcifying process is much F I G U R E 4 Mitochondrial biogenesis genes were up-regulated while combining shear stress and high phosphate treatments.…”

Section: Discussionmentioning

confidence: 85%

“…The repeated cannulation results in denudation of the intimal layer of the AVF 2 . When inspected angioscopically, the venous segment of AVF revealed detaching intima around hemodialysis needle puncture sites 2 . The hemodialysis needle puncture‐induced intimal denudation requires approximately 7–8 days to re‐endothelialize 3 .…”

Section: Introductionmentioning

confidence: 99%

“…2 When inspected angioscopically, the venous segment of AVF revealed detaching intima around hemodialysis needle puncture sites. 2 The hemodialysis needle puncture-induced intimal denudation requires approximately 7-8 days to re-endothelialize. 3 We reason that once the venous endothelium is denuded, the medial layer of the AVF is directly exposed to the blood mechanical cue (fluid shear stress) and becomes more vulnerable to the blood chemical cue (phosphate molecules).…”

Section: Introductionmentioning

confidence: 99%

“…The venous medial layer is in contact with the blood because its intima denudes. 2 Therefore, we hypothesized that upon exposure to both blood shear stress and blood phosphate, venous SMCs undergo an accelerated osteogenesis process. In this study, we aimed to elucidate the mechanical biology and pathogenesis of AVF calcification to identify the potential druggable target.…”

Section: Introductionmentioning

confidence: 99%

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Mechanical and chemical cues synergistically promote human venous smooth muscle cell osteogenesis through integrin β1‐ERK1/2 signaling: A cell model of hemodialysis fistula calcification

Yang

Chang

et al. 2021

The FASEB Journal

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Arteriovenous fistula (AVF) is the vascular access of choice for renal replacement therapy. However, AVF is susceptible to calcification with a high prevalence of 40%–65% in chronic hemodialysis patients. Repeated needle puncture for hemodialysis cannulation results in intimal denudation of AVF. We hypothesized that exposure to blood shear stress in the medial layer promotes venous smooth muscle cell (SMC) osteogenesis. While previous studies of shear stress focused on arterial‐type SMCs, SMCs isolated from the vein had not been investigated. This study established a venous cell model of AVF using the fluid shear device, combined with a high phosphate medium to mimic the uremic milieu. Osteogenic gene expression of venous SMCs upon mechanical and chemical cues was analyzed in addition to the activated cell signaling pathways. Our findings indicated that upon shear stress and high phosphate environment, mechanical stimulation (shear stress) had an additive effect in up‐regulation of an early osteogenic marker, Runx2. We further identified that the integrin β1‐ERK1/2 signaling pathway was responsible for the molecular basis of venous SMC osteogenesis upon shear stress exposure. Mitochondrial biogenesis also took part in the early stage of this venopathy pathogenesis, evident by the up‐regulated mitochondrial transcription factor A and mitochondrial DNA polymerase γ in venous SMCs. In conclusion, synergistic effects of fluid shear stress and high phosphate induce venous SMC osteogenesis via the ERK1/2 pathway through activating the mechanosensing integrin β1 signaling. The present study identified a promising druggable target for reducing AVF calcification, which deserves further in vivo investigations.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 85%