Scholarlink

<p>Ischemia-reperfusion injury (IRI) represents a significant clinical challenge characterized by mitochondrial dysfunction and redox imbalance during blood flow restoration following ischemia. This review provides a critical analysis of ozone therapy’s emerging role in IRI management through its unique hormetic properties. Recent research has transformed our understanding of ozone—traditionally considered harmful—revealing that controlled administration demonstrates remarkable therapeutic potential through dose-dependent effects. Quantitative analysis reveals that low-dose ozone exposure (10–40 µg/mL) significantly reduces oxidative stress markers while increasing antioxidant enzyme activity across multiple organ systems. The protective effects manifest primarily through enhanced Nuclear factor erythroid 2-related factor 2 activity, orchestrating upregulation of key protective enzymes while suppressing excessive nuclear factor kappa B mediated inflammation. Current evidence demonstrates consistent protective effects across cardiovascular, digestive, urogenital, and cerebral systems, with effect sizes ranging from moderate to large. However, critical analysis reveals significant limitations including predominant reliance on animal models (&gt;95% of studies), lack of standardized protocols, and limited human clinical data. Safety assessment indicates a narrow therapeutic window, with beneficial effects observed at 10–40 µg/mL but potential toxicity at doses &gt;80 µg/mL. This review establishes that while ozone therapy shows promising experimental efficacy in IRI through hormetic modulation of cellular stress responses, substantial research gaps exist regarding optimal dosing, administration protocols, and long-term safety. Future clinical translation requires rigorous standardization of therapeutic parameters, comprehensive safety assessment, and well-designed human trials to validate experimental findings.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Beyond Paradox: Ozone Therapy as a Hormetic Modulator in Ischemia-Reperfusion Injury - An Update

  • 期刊论文

  • 发表日期：

    2025年7月10日

查看全文
  • Yong Ye,
  • Zi-hang Yu,
  • Liang Nie,
  • Fei-xiang Wang,
  • Guo Mu

摘要

Ischemia-reperfusion injury (IRI) represents a significant clinical challenge characterized by mitochondrial dysfunction and redox imbalance during blood flow restoration following ischemia. This review provides a critical analysis of ozone therapy’s emerging role in IRI management through its unique hormetic properties. Recent research has transformed our understanding of ozone—traditionally considered harmful—revealing that controlled administration demonstrates remarkable therapeutic potential through dose-dependent effects. Quantitative analysis reveals that low-dose ozone exposure (10–40 µg/mL) significantly reduces oxidative stress markers while increasing antioxidant enzyme activity across multiple organ systems. The protective effects manifest primarily through enhanced Nuclear factor erythroid 2-related factor 2 activity, orchestrating upregulation of key protective enzymes while suppressing excessive nuclear factor kappa B mediated inflammation. Current evidence demonstrates consistent protective effects across cardiovascular, digestive, urogenital, and cerebral systems, with effect sizes ranging from moderate to large. However, critical analysis reveals significant limitations including predominant reliance on animal models (>95% of studies), lack of standardized protocols, and limited human clinical data. Safety assessment indicates a narrow therapeutic window, with beneficial effects observed at 10–40 µg/mL but potential toxicity at doses >80 µg/mL. This review establishes that while ozone therapy shows promising experimental efficacy in IRI through hormetic modulation of cellular stress responses, substantial research gaps exist regarding optimal dosing, administration protocols, and long-term safety. Future clinical translation requires rigorous standardization of therapeutic parameters, comprehensive safety assessment, and well-designed human trials to validate experimental findings.

Graphical Abstract