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Background <p>High-altitude hypobaric hypoxia induces inflammation and oxidative stress, yet the role of myeloperoxidase (MPO) in this pathology remains incompletely understood. This study aimed to investigate whether MPO mediates injury to the liverspleen axis under hypoxic conditions.</p> Results <p>Using a 3day murine hypoxia model, we unexpectedly found that MPO deficiency exacerbated, rather than mitigated, damage to the liverspleen axis. Compared with hypoxic wildtype mice, MPO<sup>−/−</sup> mice displayed aggravated histopathological injury, accompanied by excessive phagocyte recruitment and elevated expression of key chemokines (KC, MCP1, MIP2) and proinflammatory mediators (TNFα, IL1β, IL17A). At the molecular level, MPO absence increased splenic protein expression of NFκB, NLRP3, and iNOS, while dysregulating the antioxidant response via the NRF2/HO1 pathway.</p> Conclusions <p>These results reveal a novel protective role for MPO during hypoxic stress, where it functions to moderate the innate immune response and limit collateral tissue damage in the liverspleen axis. The study provides new insights into the complex immunomodulatory functions of MPO and suggests its activity is essential for maintaining immune homeostasis during acute hypoxia.</p>

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Myeloperoxidase regulates hypoxia-induced inflammation and oxidative stress in liver-spleen axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月2日

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  • Yonggui Li,
  • Xiaoli Liu,
  • Lingming Zhang,
  • Xiaoluan Li,
  • Zeyi Zuo,
  • Qiao Gao,
  • Qinfang Zhu

摘要

Background

High-altitude hypobaric hypoxia induces inflammation and oxidative stress, yet the role of myeloperoxidase (MPO) in this pathology remains incompletely understood. This study aimed to investigate whether MPO mediates injury to the liverspleen axis under hypoxic conditions.

Results

Using a 3day murine hypoxia model, we unexpectedly found that MPO deficiency exacerbated, rather than mitigated, damage to the liverspleen axis. Compared with hypoxic wildtype mice, MPO−/− mice displayed aggravated histopathological injury, accompanied by excessive phagocyte recruitment and elevated expression of key chemokines (KC, MCP1, MIP2) and proinflammatory mediators (TNFα, IL1β, IL17A). At the molecular level, MPO absence increased splenic protein expression of NFκB, NLRP3, and iNOS, while dysregulating the antioxidant response via the NRF2/HO1 pathway.

Conclusions

These results reveal a novel protective role for MPO during hypoxic stress, where it functions to moderate the innate immune response and limit collateral tissue damage in the liverspleen axis. The study provides new insights into the complex immunomodulatory functions of MPO and suggests its activity is essential for maintaining immune homeostasis during acute hypoxia.