High Concentrations of Uric Acid and Angiotensin II Act Additively to Produce Endothelial Injury.


Journal

Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001

Informations de publication

Date de publication:
2020
Historique:
received: 22 01 2020
revised: 22 02 2020
accepted: 10 03 2020
entrez: 23 6 2020
pubmed: 23 6 2020
medline: 10 7 2021
Statut: epublish

Résumé

Renin angiotensin (Ang) system (RAS) activation in metabolic syndrome (MS) patients is associated with elevated uric acid (UA) levels, resulting in endothelial system dysfunction. Our previous study demonstrated that excessive UA could cause endothelial injury through the aldose reductase (AR) pathway. This study is the first to show that a high concentration of Ang II in human umbilical vein endothelial cells (HUVECs) increases reactive oxygen species (ROS) components, including O

Identifiants

pubmed: 32565731
doi: 10.1155/2020/8387654
pmc: PMC7261330
doi:

Substances chimiques

Reactive Oxygen Species 0
von Willebrand Factor 0
Angiotensin II 11128-99-7
Uric Acid 268B43MJ25
Nitric Oxide 31C4KY9ESH
Hydrogen Peroxide BBX060AN9V
Superoxide Dismutase EC 1.15.1.1
NADPH Oxidases EC 1.6.3.-
Oxygen S88TT14065

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

8387654

Informations de copyright

Copyright © 2020 Quan Hong et al.

Déclaration de conflit d'intérêts

The authors declare that they have no competing financial interests.

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Auteurs

Quan Hong (Q)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Liyuan Wang (L)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.
Kidney Department, Halison International Peace Hospital, Hengshui City 053000, China.

Zhiyong Huang (Z)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.
Department of Nephrology, The 175th Hospital of PLA, Zhangzhou Fujian 036300, China.

Zhe Feng (Z)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Shaoyuan Cui (S)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Bo Fu (B)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Guangyan Cai (G)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Xiangmei Chen (X)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

Di Wu (D)

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Chinese PLA General Hospital, Beijing 100853, China.

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Classifications MeSH