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<p>Ferroptosis has been increasingly implicated in the pathophysiology of asthma. Glutathione peroxidase 4 (GPX4), the key enzymatic suppressor of ferroptosis, has a role in asthma that remains insufficiently defined. Here, we investigated the regulatory function of GPX4 in asthma airway epithelial cells using an OVA-induced murine model in conjunction with a lipopolysaccharide (LPS)-stimulated BEAS-2B cell system. Upregulation of GPX4 markedly reduced intracellular reactive oxygen species (ROS), malondialdehyde (MDA) levels, and the accumulation of ferrous ions and other ferroptosis-related markers, while concomitantly alleviating mitochondrial abnormalities in LPS-stimulated BEAS-2B cells. GPX4 also inhibited ERK phosphorylation and downregulated 5-lipoxygenase (5-LO) expression. In OVA-induced asthmatic mice, GPX4 conferred significant protection, characterized by alleviated lung histopathological damage, reduced inflammatory responses, and attenuation of ferroptosis-associated alterations.</p><p>These findings indicate that GPX4 mitigates asthma-related pathological changes primarily through suppression of 5-LO and modulation of ferroptosis-linked oxidative injury, highlighting GPX4 as a potential therapeutic target for asthma management.</p>

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GPX4 alleviates airway inflammation by suppressing 5-LO expression and regulating ferroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月25日

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  • Zehong Chen,
  • Jihao Cai,
  • Shijia Wang,
  • Wei Yu,
  • Feifei Yu,
  • Ruimin Zhou,
  • Chang Cai

摘要

Ferroptosis has been increasingly implicated in the pathophysiology of asthma. Glutathione peroxidase 4 (GPX4), the key enzymatic suppressor of ferroptosis, has a role in asthma that remains insufficiently defined. Here, we investigated the regulatory function of GPX4 in asthma airway epithelial cells using an OVA-induced murine model in conjunction with a lipopolysaccharide (LPS)-stimulated BEAS-2B cell system. Upregulation of GPX4 markedly reduced intracellular reactive oxygen species (ROS), malondialdehyde (MDA) levels, and the accumulation of ferrous ions and other ferroptosis-related markers, while concomitantly alleviating mitochondrial abnormalities in LPS-stimulated BEAS-2B cells. GPX4 also inhibited ERK phosphorylation and downregulated 5-lipoxygenase (5-LO) expression. In OVA-induced asthmatic mice, GPX4 conferred significant protection, characterized by alleviated lung histopathological damage, reduced inflammatory responses, and attenuation of ferroptosis-associated alterations.

These findings indicate that GPX4 mitigates asthma-related pathological changes primarily through suppression of 5-LO and modulation of ferroptosis-linked oxidative injury, highlighting GPX4 as a potential therapeutic target for asthma management.