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<p>Cardiovascular diseases (CVDs) are among the leading causes of death worldwide, and their pathogenesis is closely associated with the imbalance of the oxidative stress microenvironment. Hydrogen (H<sub>2</sub>) has attracted attention in the field of CVDs treatment due to its property of selectively scavenging reactive oxygen species (ROS) and regulating redox homeostasis. This article systematically reviews the multi-level regulatory mechanisms of H<sub>2</sub> in CVDs, including the activation of the Nrf2-Keap1 pathway, the regulation of AMPK/mTOR and JAK-STAT networks, as well as the inhibition of key pathways such as miR-124-3p-calpain, NOX4/NLRP3, Wnt/CX3CR1, and LOX-1/NF-κB, thereby participating in the remodeling of cellular redox balance. In addition to scavenging ROS, H<sub>2</sub> also exhibits certain anti-inflammatory effects, differing functionally from traditional antioxidants. This article explores the role of H<sub>2</sub> in reconstructing oxidative stress regulation, analyzes the heterogeneity of the oxidative stress microenvironment in CVDs, and provides a basis for its therapeutic potential. Integrating preclinical research and translational medicine evidence, this article proposes a "precision H<sub>2</sub> medicine" framework, aiming to provide theoretical references for targeted therapy of CVDs and explore potential pathways for precision treatment.</p>

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H2 as a potential redox homeostasis modulator: a review of mechanisms targeting key elements of cardiovascular pathogenesis-related pathways

  • 期刊论文

  • 发表日期：

    2025年11月19日

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  • Wanrong Wang,
  • Fusen Yang,
  • Biao Geng,
  • Hui Song,
  • Yue Gao,
  • Jingfei Shi,
  • Gang Wang,
  • Chao Cui

摘要

Cardiovascular diseases (CVDs) are among the leading causes of death worldwide, and their pathogenesis is closely associated with the imbalance of the oxidative stress microenvironment. Hydrogen (H2) has attracted attention in the field of CVDs treatment due to its property of selectively scavenging reactive oxygen species (ROS) and regulating redox homeostasis. This article systematically reviews the multi-level regulatory mechanisms of H2 in CVDs, including the activation of the Nrf2-Keap1 pathway, the regulation of AMPK/mTOR and JAK-STAT networks, as well as the inhibition of key pathways such as miR-124-3p-calpain, NOX4/NLRP3, Wnt/CX3CR1, and LOX-1/NF-κB, thereby participating in the remodeling of cellular redox balance. In addition to scavenging ROS, H2 also exhibits certain anti-inflammatory effects, differing functionally from traditional antioxidants. This article explores the role of H2 in reconstructing oxidative stress regulation, analyzes the heterogeneity of the oxidative stress microenvironment in CVDs, and provides a basis for its therapeutic potential. Integrating preclinical research and translational medicine evidence, this article proposes a "precision H2 medicine" framework, aiming to provide theoretical references for targeted therapy of CVDs and explore potential pathways for precision treatment.