Hyperuricemia: A key contributor to endothelial dysfunction in cardiovascular diseases

Author:

Wei Xin123,Zhang Mao23,Huang Shian23,Lan Xiaozhong4,Zheng Jing5,Luo Hui6,He Yuan12,Lei Wei1ORCID

Affiliation:

1. Guangdong Provincial Engineering Technology Research Center for Molecular Diagnosis and Innovative Drugs Translation of Cardiopulmonary Vascular Diseases, University Joint Laboratory of Guangdong Province and Macao Region on Molecular Targets and Intervention of Cardiovascular Diseases, Department of Precision Laboratory Affiliated Hospital of Guangdong Medical University Zhanjiang China

2. Laboratory of Cardiovascular Diseases Affiliated Hospital of Guangdong Medical University Zhanjiang China

3. Cardiovascular Medicine Center Affiliated Hospital of Guangdong Medical University Zhanjiang China

4. TAAHC‐GDMU Biomedical and Health Joint R&D Center, The Provincial and Ministerial Co‐founded Collaborative Innovation Center for R&D in Tibet Characteristic Agriculture and Animal Husbandry Resources, The Center for Xizang Chinese (Tibetan) Medicine Resource, Joint Laboratory for Tibetan Materia Medica Resource Scientific Protection and Utilization, Tibetan Medical Research Center of Tibet Tibet Agriculture and Animal Husbandry University Nyingchi, Tibet China

5. Department of Obstetrics and Gynecology University of Wisconsin Wisconsin Madison USA

6. Southern Marine Science and Engineering Guangdong Laboratory‐Zhanjiang The Marine Biomedical Research Institute, Guangdong Medical University Zhanjiang China

Abstract

AbstractAs an end product of purine metabolism, uric acid (UA) is a major endogenous antioxidant in humans. However, impaired UA synthesis and excretion can lead to hyperuricemia (HUA), which may in turn induce endothelial dysfunction (ED) and contribute to the pathogenesis of cardiovascular diseases (CVDs; e.g., atherosclerosis and hypertension). In this review, we discuss recent advances and novel insights into the effects exerted by HUA conditions in ED and related underlying mechanisms focusing on impaired UA metabolism, reduction in the synthesis and bioavailability of nitric oxide, endothelial cell injury, the endothelial‐to‐mesenchymal transition, insulin resistance, procoagulant activity, and acquisition of an inflammatory phenotype. We additionally discuss intervention strategies for HUA‐induced ED and the paradoxical roles of UA in endothelial function. We summarize major conclusions and perspectives: the deleterious effects of HUA contribute to the initiation and progression of CVD‐related ED. However, the treatment strategies (in addition to urate‐lowering therapy) for increasing endothelial function are limited because the majority of literature on pharmacological and pathophysiological mechanisms underlying HUA‐induced ED solely describes in vitro models. Therefore, a better understanding of the mechanisms involved in HUA‐induced ED is critical to the development of novel therapies for preventing and treating CVD‐HUA comorbidities.

Funder

National Natural Science Foundation of China

Zhanjiang Science and Technology Bureau

Natural Science Foundation of Guangdong Province

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

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