Hyperuricemia: A key contributor to endothelial dysfunction in cardiovascular diseases

Area of Science:

• Biochemistry
• Cardiovascular Research
• Endocrinology

Background:

• Uric acid (UA) is a byproduct of purine metabolism and an endogenous antioxidant.
• Impaired UA metabolism can lead to hyperuricemia (HUA), a condition linked to endothelial dysfunction (ED) and cardiovascular diseases (CVDs).

Purpose of the Study:

• To review recent advances in understanding HUA's effects on ED.
• To explore underlying mechanisms and potential intervention strategies for HUA-induced ED.

Main Methods:

• Literature review focusing on HUA's impact on endothelial function.
• Analysis of mechanisms including nitric oxide reduction, endothelial cell injury, and inflammatory responses.

Main Results:

• HUA contributes to the initiation and progression of CVD-related ED.
• Mechanisms involve impaired UA metabolism, reduced nitric oxide bioavailability, endothelial cell injury, endothelial-to-mesenchymal transition, insulin resistance, procoagulant activity, and inflammation.

Conclusions:

• HUA plays a deleterious role in endothelial function and CVD pathogenesis.
• Current treatment strategies are limited, with most research relying on in vitro models.
• Further research into HUA-induced ED mechanisms is crucial for novel therapeutic development.