机构:[1]Vascular Biology and Therapeutics Program and the Department of Surgery, Yale School of Medicine, Yale University, New Haven, USA.[2]The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.[3]Department of Vascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.[4]Department of Vascular Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.外科系统血管外科首都医科大学宣武医院[5]Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, China.医技科室血管超声科首都医科大学宣武医院[6]Section of Vascular and Endovascular Surgery, VA Connecticut Healthcare System, West Haven, USA.
The increasing prevalence of chronic and end-stage renal disease creates an increased need for reliable vascular access, and although arteriovenous fistulae (AVF) are the preferred mode of hemodialysis access, 60% fail to mature and only 50% remain patent at one year. Fistulae mature by diameter expansion and wall thickening; this outward remodeling of the venous wall in the fistula environment relies on a delicate balance of extracellular matrix (ECM) remodeling, inflammation, growth factor secretion, and cell adhesion molecule upregulation in the venous wall. AVF failure occurs via two distinct mechanisms with early failure secondary to lack of outward remodeling, that is insufficient diameter expansion or wall thickening, whereas late failure occurs with excessive wall thickening due to neointimal hyperplasia (NIH) and insufficient diameter expansion in a previously functional fistula. In recent years, the molecular basis of AVF maturation and failure are becoming understood in order to develop potential therapeutic targets to aide maturation and prevent access loss. Erythropoietin-producing hepatocellular carcinoma (Eph) receptors, along with their ligands, ephrins, determine vascular identity and are critical for vascular remodeling in the embryo. Manipulation of Eph receptor signaling in adults, as well as downstream pathways, is a potential treatment strategy to improve the rates of AVF maturation and patency. This review examines our current understanding of molecular changes occurring following fistula creation, factors predictive of fistula success, and potential areas of intervention to decrease AVF failure.
基金:
Association of VA
Surgeons Resident Research Award [J.G.], the National
Institutes of Health R01-HL128406 and R01-HL144476
[A.D.], as well as with the resources and the use of
facilities at the VA Connecticut Healthcare System, West
Haven, CT.
语种:
外文
PubmedID:
第一作者:
第一作者机构:[1]Vascular Biology and Therapeutics Program and the Department of Surgery, Yale School of Medicine, Yale University, New Haven, USA.
通讯作者:
通讯机构:[1]Vascular Biology and Therapeutics Program and the Department of Surgery, Yale School of Medicine, Yale University, New Haven, USA.[6]Section of Vascular and Endovascular Surgery, VA Connecticut Healthcare System, West Haven, USA.[*1]Yale University School of Medicine, Department of Surgery and of Cellular and Molecular Physiology, 10 Amistad Street, Room 437, PO Box 208089, New Haven, CT 06520-8089, USA.
推荐引用方式(GB/T 7714):
Gorecka Jolanta,Fereydooni Arash,Gonzalez Luis,et al.Molecular Targets for Improving Arteriovenous Fistula Maturation and Patency.[J].Vascular Investigation And Therapy.2019,2(2):33-41.doi:10.4103/VIT.VIT_9_19.
APA:
Gorecka Jolanta,Fereydooni Arash,Gonzalez Luis,Lee Shin Rong,Liu Shirley...&Dardik Alan.(2019).Molecular Targets for Improving Arteriovenous Fistula Maturation and Patency..Vascular Investigation And Therapy,2,(2)
MLA:
Gorecka Jolanta,et al."Molecular Targets for Improving Arteriovenous Fistula Maturation and Patency.".Vascular Investigation And Therapy 2..2(2019):33-41