The harmful effect of indoxyl sulfate on neovascularization in chronic kidney disease

被引:12
作者
Dou, Laetitia [1 ]
Burtey, Stephane [1 ,2 ]
机构
[1] Aix Marseille Univ, INSERM, Vasc Res Ctr Marseille, UMR S 1076, F-13005 Marseille, France
[2] Ctr Nephrol Dialyse Transplantat Renale, CHU Concept, Assistance Publ Hop Marseille, Marseille, France
关键词
ARTERY-DISEASE; UREMIC TOXINS; INJURY; CKD;
D O I
10.1016/j.kint.2015.12.030
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Patients with chronic kidney disease display an impairment of neovascularization in ischemic tissues. Studies have suggested the involvement of the uremic toxin indoxyl sulfate by demonstrating that indoxyl sulfate affects endothelial progenitor cells. However, few data are available on the effects of indoxyl sulfate on neovascularization and on the mechanisms involved. The article by Hung et al. shows that indoxyl sulfate suppresses neovascularization in uremic mice by impairing endothelial progenitor cell function via the inhibition of hypoxia-induced hypoxia-inducible factor/interleukin-10/vascular endothelial growth factor signaling. (C) 2016 International Society of Nephrology
引用
收藏
页码:532 / 534
页数:3
相关论文
共 9 条
[1]  
Asai H, 2015, AM J PHYSL CELL PHYS
[2]   Peripheral Artery Disease and CKD: A Focus on Peripheral Artery Disease as a Critical Component of CKD Care [J].
Garimella, Pranav S. ;
Hart, Peter D. ;
O'Hare, Ann ;
DeLoach, Stephanie ;
Herzog, Charles A. ;
Hirsch, Alan T. .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2012, 60 (04) :641-654
[3]   Indoxyl sulfate suppresses endothelial progenitor cell-mediated neovascularization [J].
Hung, Szu-Chun ;
Kuo, Ko-Lin ;
Huang, Hsin-Lei ;
Lin, Chia-Chun ;
Tsai, Tung-Hu ;
Wang, Chao-Hung ;
Chen, Jaw-Wen ;
Lin, Shing-Jong ;
Huang, Po-Hsun ;
Tarng, Der-Cherng .
KIDNEY INTERNATIONAL, 2016, 89 (03) :574-585
[4]   Vascular Incompetence in Dialysis Patients-Protein-Bound Uremic Toxins and Endothelial Dysfunction [J].
Jourde-Chiche, Noemie ;
Dou, Laetitia ;
Cerini, Claire ;
Dignat-George, Francoise ;
Brunet, Philippe .
SEMINARS IN DIALYSIS, 2011, 24 (03) :327-337
[5]   Hepatic Sulfotransferase as a Nephropreventing Target by Suppression of the Uremic Toxin Indoxyl Sulfate Accumulation in Ischemic Acute Kidney Injury [J].
Saito, Hideyuki ;
Yoshimura, Misato ;
Saigo, Chika ;
Komori, Megumi ;
Nomura, Yui ;
Yamamoto, Yuko ;
Sagata, Masataka ;
Wakida, Ayaka ;
Chuman, Erina ;
Nishi, Kazuhiko ;
Jono, Hirofumi .
TOXICOLOGICAL SCIENCES, 2014, 141 (01) :206-217
[6]   The Aryl Hydrocarbon Receptor-Activating Effect of Uremic Toxins from Tryptophan Metabolism: A New Concept to Understand Cardiovascular Complications of Chronic Kidney Disease [J].
Sallee, Marion ;
Dou, Laetitia ;
Cerini, Claire ;
Poitevin, Stephane ;
Brunet, Philippe ;
Burtey, Stephane .
TOXINS, 2014, 6 (03) :934-949
[7]   A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: Renal insufficiency is associated with poor coronary collateral vessel development [J].
Sezer, Murat ;
Onan, Mustafa ;
Okcular, Irem ;
Elitok, Ali ;
Umman, Sabahattin ;
Umman, Berrin ;
Tayyareci, Yelda ;
Olcay, Ayhan ;
Nisanci, Yilmaz ;
Bilge, Ahmet Kaya ;
Meric, Mehmet .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 2007, 115 (03) :366-372
[8]   Indoxyl sulfate signals for rapid mRNA stabilization of Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) and suppresses the expression of hypoxia-inducible genes in experimental CKD and uremia [J].
Tanaka, Tetsuhiro ;
Yamaguchi, Junna ;
Higashijima, Yoshiki ;
Nangaku, Masaomi .
FASEB JOURNAL, 2013, 27 (10) :4059-4075
[9]   In acute kidney injury, indoxyl sulfate impairs human endothelial progenitor cells: modulation by statin [J].
Wu, Vin-Cent ;
Young, Guang-Huar ;
Huang, Po-Hsun ;
Lo, Shyh-Chyi ;
Wang, Kuo-Chuan ;
Sun, Chiao-Yin ;
Liang, Chan-Jung ;
Huang, Tao-Ming ;
Chen, Jou-Han ;
Chang, Fan-Chi ;
Chen, Yuh-Lien ;
Kuo, Yih-Shing ;
Chen, Jin-Bor ;
Chen, Jaw-Wen ;
Chen, Yung-Ming ;
Ko, Wen-Jo ;
Wu, Kwan-Dun .
ANGIOGENESIS, 2013, 16 (03) :609-624