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Objectives <p>To evaluate whether oxygen–ozone therapy (OOT) can modulate aging by inducing adaptive chaos in the HMGB1–Nrf2 redox-inflammatory pathway.</p> Methods <p>A computational systems biology model simulated feedback loops among ROS, Nrf2, HMGB1, and NF-κB under varying ozone doses and cellular contexts (protective vs. autophagy-deficient).</p> Results <p>Intermediate ozone doses in the model triggered controlled chaos. The model suggests a potential 'chaotic window' (30–40&#xa0;μg/mL ozone) that may promote redox resilience in autophagy-deficient cells.</p> Conclusion <p>OOT may potentially contribute to healthy aging by modulating redox adaptability. Its theoretical effectiveness is dose-dependent, with maximal benefit in aged or dysfunctional systems requiring reactivation of flexible stress responses. However, while the model offers insights into possible dynamic behaviours of the redox-inflammatory axis under ozone exposure, it is not yet calibrated to biological data and cannot predict real-world outcomes without further experimental support.</p>

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A conceptual model of oxygen–ozone therapy as a modulator of aging via the HMGB1 pathway

  • 期刊论文

  • 发表日期：

    2025年12月23日

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  • Salvatore Chirumbolo,
  • Luigi Valdenassi,
  • Dario Bertossi,
  • Fortunato Loprete,
  • Umberto Tirelli,
  • Marianno Franzini

摘要

Objectives

To evaluate whether oxygen–ozone therapy (OOT) can modulate aging by inducing adaptive chaos in the HMGB1–Nrf2 redox-inflammatory pathway.

Methods

A computational systems biology model simulated feedback loops among ROS, Nrf2, HMGB1, and NF-κB under varying ozone doses and cellular contexts (protective vs. autophagy-deficient).

Results

Intermediate ozone doses in the model triggered controlled chaos. The model suggests a potential 'chaotic window' (30–40 μg/mL ozone) that may promote redox resilience in autophagy-deficient cells.

Conclusion

OOT may potentially contribute to healthy aging by modulating redox adaptability. Its theoretical effectiveness is dose-dependent, with maximal benefit in aged or dysfunctional systems requiring reactivation of flexible stress responses. However, while the model offers insights into possible dynamic behaviours of the redox-inflammatory axis under ozone exposure, it is not yet calibrated to biological data and cannot predict real-world outcomes without further experimental support.