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MINI REVIEW article

Front. Immunol.

Sec. Inflammation

This article is part of the Research TopicInflammation, Immunity, and Cancer: New Pathways Towards Therapeutic InnovationView all 15 articles

Ferroptosis in Sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): A Potential Therapeutic Strategy

Provisionally accepted
Lingling  WangLingling WangWenzhe  ZhangWenzhe ZhangXiujing  FengXiujing Feng*
  • Shandong First Medical University, Jinan, China

The final, formatted version of the article will be published soon.

Sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS) remains a devastating complication of sepsis, marked by uncontrolled pulmonary inflammation, alveolar–capillary barrier disruption, and high mortality. Despite advances in supportive care, no targeted medicines are currently available. Ferroptosis is an iron-dependent and non-apoptotic form of cell death characterized by the iron induced accumulation of lipid reactive oxygen species (ROS). Emerging evidence indicates that ferroptosis is involved in the progression of sepsis induced ALI/ARDS, although the mechanism of action of ferroptosis in sepsis induced ALI/ARDS is still poorly understood. This mini-review summarizes the mechanism of ferroptosis action on sepsis induced ALI/ARDS, with particular focus on immune dysregulation, endothelial/epithelial dysfunction, and oxidative stress. We highlight key molecular pathways, including glutathione peroxidase 4 (GPX4) inactivation, iron metabolism disruption, and lipid peroxidation cascades, supported by both preclinical studies and emerging clinical correlates. Furthermore, discuss the potential therapeutic approaches currently used to treat ARDS. This review also discusses major challenges to clinical translation and highlights further directions for the treatment and prevention of sepsis induced ALI/ARDS.

Keywords: ferroptosis, Sepsis induced acute lung injury/acute respiratory distress syndrome, therapeutic strategy, Immune Regulation, Oxidative Stress

Received: 20 Aug 2025; Accepted: 13 Nov 2025.

Copyright: © 2025 Wang, Zhang and Feng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Xiujing Feng, fengxj@nju.edu.cn

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