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Purpose <p>This review aims to explore the role of hyperuricemia in the pathogenesis of hypoxic pulmonary hypertension (HPH), focusing on its contribution to pulmonary vascular remodeling and evaluating the potential of uric acid-lowering strategies.</p> Methods <p>A comprehensive review of the literature was conducted to assess the impact of elevated uric acid levels on HPH. The review highlights uric acid’s effects on smooth muscle cell proliferation, endothelial dysfunction, oxidative stress, and inflammation. It also examines the interference of uric acid with nitric oxide signaling and its activation of the renin-angiotensin system under hypoxic conditions.</p> Results <p>The literature indicates a significant correlation between elevated serum uric acid levels and the severity of HPH. Uric acid contributes to vascular remodeling by promoting oxidative stress, inflammation, and endothelial dysfunction. Preclinical evidence suggests that uric acid-lowering interventions, when combined with antioxidant or anti-inflammatory therapies, may reduce pulmonary vascular damage and improve outcomes.</p> Conclusion <p>Uric acid represents a potential therapeutic target for HPH. Uric acid-lowering strategies, although promising, require further clinical validation. A deeper understanding of the molecular mechanisms underlying hyperuricemia in HPH may facilitate the development of targeted diagnostic and therapeutic approaches.</p>

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Hyperuricemia and Hypoxic Pulmonary Hypertension: Pathogenic Links, Clinical Evidence, and Emerging Therapeutic Insights

  • 期刊论文

  • 发表日期：

    2026年3月6日

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  • Zhanpeng Cao,
  • Wei Ma,
  • Chuanchuan Liu

摘要

Purpose

This review aims to explore the role of hyperuricemia in the pathogenesis of hypoxic pulmonary hypertension (HPH), focusing on its contribution to pulmonary vascular remodeling and evaluating the potential of uric acid-lowering strategies.

Methods

A comprehensive review of the literature was conducted to assess the impact of elevated uric acid levels on HPH. The review highlights uric acid’s effects on smooth muscle cell proliferation, endothelial dysfunction, oxidative stress, and inflammation. It also examines the interference of uric acid with nitric oxide signaling and its activation of the renin-angiotensin system under hypoxic conditions.

Results

The literature indicates a significant correlation between elevated serum uric acid levels and the severity of HPH. Uric acid contributes to vascular remodeling by promoting oxidative stress, inflammation, and endothelial dysfunction. Preclinical evidence suggests that uric acid-lowering interventions, when combined with antioxidant or anti-inflammatory therapies, may reduce pulmonary vascular damage and improve outcomes.

Conclusion

Uric acid represents a potential therapeutic target for HPH. Uric acid-lowering strategies, although promising, require further clinical validation. A deeper understanding of the molecular mechanisms underlying hyperuricemia in HPH may facilitate the development of targeted diagnostic and therapeutic approaches.