Impact of Indoxyl Sulfate on Progenitor Cell-Related Neovascularization of Peripheral Arterial Disease and Post-Angioplasty Thrombosis of Dialysis Vascular Access.

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vascular disease 4 angiologydiseases
ischemia 2 angiologydiseases
peripheral artery disease 2 angiologydiseases
thrombosis 23 angiologydiseases

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ischemia 8858 vessels from pre-existing vascular structures, is an essential physiological process to cope with tissue ischemia . The ability of collateral vessel formation in ischemic tissues is decreased in patients with CKD [[39]].
ischemia 11657 group, the indole group, and the indole plus AST-120 group. Eight weeks later, unilateral hindlimb ischemia (HI) surgery was performed on all animals. At Week 2 and Week 4 after HI surgery, the blood flow recovery
peripheral artery disease 1924 have indicated that in addition to coronary and cerebral arteries, indoxyl sulfate plays a role in peripheral artery disease (PAD) and dialysis graft thrombosis. Emerging evidence suggests that indoxyl sulfate is implicated via
peripheral artery disease 2910 in patients with CKD [[1],[2],[3],[4],[5],[6]]. In addition to cerebral and coronary artery disease, peripheral artery disease (PAD) is highly prevalent among patients with CKD [[7]]. Creation of vascular accesses for dialysis,
thrombosis 1975 cerebral arteries, indoxyl sulfate plays a role in peripheral artery disease (PAD) and dialysis graft thrombosis . Emerging evidence suggests that indoxyl sulfate is implicated via novel mechanisms, including progenitor
thrombosis 3176 (AVFs) and prosthetic arteriovenous grafts (AVGs), is also frequently associated with stenosis and thrombosis [[8],[9]]. Although traditional vascular risk factors are common in patients with CKD, they cannot sufficiently
thrombosis 4871 percutaneous transluminal angioplasty (PTA) can achieve a high success rate, recurrent stenosis and thrombosis are usually inevitable. At one year after PTA, only 26%–58% of native fistulas remain functional without
thrombosis 5172 of native fistulas, as only 40%–50% of AVGs remain functional at six months after intervention. If thrombosis develops in AVGs, the three-month unassisted patency rate ranges from 30% to 40% [[13]]. As a result,
thrombosis 7366 abnormal vascular repair and neointima hyperplasia (Table 1).In addition to the above pathways, pro- thrombosis and angiogenesis have been discovered in recent studies as novel mechanisms by which indoxyl sulfate
thrombosis 7596 dysfunction. In this review, we focus on the effect of indoxyl sulfate on the angiogenesis of PAD and thrombosis of dialysis vascular accesses.3. Indoxyl Sulfate and Progenitor Cell-Related Neovascularization3.1.
thrombosis 12702 common cause of secondary vascular access failure [[46]]. According to Virchow’s triad, vascular thrombosis involves an interplay among blood stasis, vessel injury, and hypercoagulability [[47]]. A major predisposing
thrombosis 12833 interplay among blood stasis, vessel injury, and hypercoagulability [[47]]. A major predisposing factor for thrombosis of vascular accesses is stenoses in the outflow veins, which cause blood stasis and are noted in 60%–80%
thrombosis 13105 still occur in the absence of stenosis. In addition, not all vascular accesses with stenoses experience thrombosis ; thus, there must be other factors contributing to thrombosis. For example, low-flow state secondary
thrombosis 13167 vascular accesses with stenoses experience thrombosis; thus, there must be other factors contributing to thrombosis . For example, low-flow state secondary to hypotension has been proposed to precipitate thrombosis [[48]].
thrombosis 13265 to thrombosis. For example, low-flow state secondary to hypotension has been proposed to precipitate thrombosis [[48]]. Other causes, such as vascular injury, inflammation, and inadequate hemostasis of dialysis accesses,
thrombosis 13441 inadequate hemostasis of dialysis accesses, may also precipitate the development of vascular access thrombosis [[49]]. Previous studies have demonstrated a prothrombotic state in patients on hemodialysis [[1],[2],[50],[51],[52],[53]].
thrombosis 13675 Both inherited and acquired thrombophilia have been reported as possible causes of dialysis access thrombosis [[54],[55],[56]]. Nonetheless, neither antiplatelet drugs nor anticoagulants have a significant effect.Recently,
thrombosis 13855 anticoagulants have a significant effect.Recently, indoxyl sulfate was implicated in the increased risk of thrombosis in patients on hemodialysis. In a study on 100 patients on hemodialysis without vascular access dysfunction,
thrombosis 14218 patients with vascular access dysfunction, baseline serum indoxyl sulfate levels were associated with thrombosis of vascular accesses after endovascular interventions [[57]]. A total of 175 patients with graft accesses
thrombosis 14981 of Indoxyl Sulfate on ThrombosisBlood stasis secondary to stenoses is the most common mechanism for thrombosis of dialysis vascular accesses. Nonetheless, the role of indoxyl sulfate in stenoses of dialysis vascular
thrombosis 15897 cells and vascular smooth muscle cells [[32],[33]]. Tissue factor is a crucial mediator of vascular thrombosis . Using a de-endothelialized, postinterventional model, Chitalia et al. exposed human vascular smooth
thrombosis 16824 suggest that indoxyl sulfate and AHR may comprise a promising therapeutic platform to treat or prevent thrombosis in patients with CKD [[34]].An intact endothelium possesses both anti-platelet and anti-thrombotic properties.
thrombosis 17083 is highly thrombogenic. Therefore, re-endothelialization may be another critical factor related to thrombosis after endovascular therapy. Indoxyl sulfate inhibits endothelial proliferation and impairs wound repair
thrombosis 17478 [[61]]. Clinical studies have shown progenitor cell deficiency to be associated with restenosis and thrombosis after endovascular intervention [[62],[63],[64]]. Indoxyl sulfate has a deleterious effect on progenitor
thrombosis 17631 [[62],[63],[64]]. Indoxyl sulfate has a deleterious effect on progenitor cell function, which may precipitate thrombosis through delayed re-endothelialization [[36]]. Nonetheless, the link among indoxyl sulfate, re-endothelialization
thrombosis 17759 re-endothelialization [[36]]. Nonetheless, the link among indoxyl sulfate, re-endothelialization and thrombosis still remains unclear. The possible pro-thrombotic mechanisms of indoxyl sulfate are summarized in Figure
thrombosis 18932 vascular endothelial growth factor).Figure 2Possible mechanisms of indoxyl sulfate induction of vascular thrombosis . EC, endothelial cell; EPC, endothelial progenitor cell; IS, indoxyl sulfate, TF, tissue factor; VSMC,
vascular disease 1111 date (collection): 1/2017AbstractPatients with chronic kidney disease (CKD) have an increased risk of vascular disease , which is associated with considerable health care costs. Vascular disease in CKD differs clinically
vascular disease 1401 Besides the traditional risk factors, retention of uremic toxins contributes to the pathogenesis of vascular disease in patients with CKD. Indoxyl sulfate is a protein-bound uremic toxin and is inefficiently removed by
vascular disease 2592 kidney function, patients with chronic kidney disease (CKD) are more likely to develop atherosclerotic vascular disease . Vascular disease-related ischemic events cause significant morbidity and mortality in patients with
vascular disease 3392 sufficiently account for the increased vascular events [[2]]. Understanding the unique pathophysiology of vascular disease in patients with CKD may help to develop strategies for prevention and therapy. In the following sections,

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