ArticleInflammation2024
Iron Overload-Dependent Ferroptosis Aggravates LPS-Induced Acute Lung Injury by Impairing Mitochondrial Function.
Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The trial behind it
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Who cites it
29 citing papers in PubMed.
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2027Review
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- Iron and Other Metal Ions in Human Health and Disease.MedComm · 2026Review
- A Huaxian Formula Nanoformulation Confers Protection Against Acute Radiation-Induced Lung Injury by Targeting Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ferroptosis-Senescence Crosstalk in Sepsis-Associated Acute Lung Injury: Mechanisms and Therapeutic Opportunities.Biomedicines · 2026Review
- Light-Inducible Bispecific DNAzymes Reveal Mitochondrial FeAngewandte Chemie (International ed. in English) · 2026Article
- Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Linking Gut Microbiota, Mitochondrial Redox Dysfunction, and Ferroptosis in Cardiometabolic Diseases: A Narrative Review of Mechanistic Evidence and Redox-Targeted Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- The RAGE-Ferroptosis Axis Drives Oxidative Stress-Associated Inflammatory Lung Injury in Viral Infection.Antioxidants (Basel, Switzerland) · 2026Article
- Multifunctional fluorescent carbon dots with synergistic-mechanism targeted mitochondria and Fe³⁺ detection.Mikrochimica acta · 2026Article
- Targeting Hsp70 triggers ferroptosis: a novel anti-cancer mechanism of a marine natural product in prostate cancer.Natural products and bioprospecting · 2026Article
- Article
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics.Frontiers in immunology · 2026Review
- MitoQ in sepsis-associated acute lung injury: redox pharmacology, mechanistic evidence, and translational perspectives.Frontiers in pharmacology · 2026Review
- Inhalable targeted CD8 + T cell nanoparticles loaded ferroptosis inhibitor ferrostatin-1 alleviate acute lung injury.Journal of nanobiotechnology · 2025Article
- Therapeutic potential of traditional Chinese medicine and mechanisms for the treatment of type 2 diabetes mellitus.Chinese medicine · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Ferroptosis is a newly proposed form of programmed cell death that is iron-dependent and closely linked to oxidative stress. Its specific morphological changes include shrunken mitochondria, increased density of mitochondrial membrane, and rupture or disappearance of mitochondrial cristae. The main mechanism of ferroptosis involves excessive free iron reacting with membrane phospholipids, known as the Fenton reaction, resulting in lipid peroxidation. However, the role of iron in acute lung injury (ALI) remains largely unknown. In this study, LPS was instilled into the airway to induce ALI in mice. We observed a significant increase in iron concentration during ALI, accompanied by elevated levels of lipid peroxidation markers such as malonaldehyde (MDA) and 4-hydroxynonenal (4-HNE). Treatment with the iron chelator deferoxamine (DFO) or ferroptosis inhibitor ferrostatin-1 (Fer-1) reversed lipid peroxidation and significantly attenuates lung injury. Similarly, DFO or Fer-1 treatment improved the cell survival significantly in vitro. These results demonstrated that ferroptosis occurs during ALI and that targeting ferroptosis is an effective treatment strategy. Interestingly, we found that the increased iron was primarily concentrated in mitochondria and DFO treatment effectively restored normal mitochondria morphology. To further confirm the damaging effect of iron on mitochondria, we performed mitochondrial stress tests in vitro, which revealed that iron stimulation led to mitochondrial dysfunction, characterized by impaired basal respiratory capacity, ATP production capacity, and maximum respiratory capacity. MitoTEMPO, an antioxidant targeting mitochondria, exhibited superior efficacy in improving iron-induced mitochondrial dysfunction compared to the broad-spectrum antioxidant NAC. Treatment with MitoTEMPO more effectively alleviated ALI. In conclusion, ferroptosis contributes to the pathogenesis of ALI and aggravates ALI by impairing mitochondrial function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.