ArticleClinical proteomics2025
Dimethyl fumarate alleviates inflammation during high altitude hypoxia induced acute lung injury by upregulating Nrf2/SLC7A11 pathway in ferroptosis.
Article in Clinical proteomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Emerging Role of Dimethyl Fumarate in Alzheimer's Disease-A Systematic Review of Available Preclinical Studies.International journal of molecular sciences · 2026Pooled it
- Chronic hypoxia adaptation at high altitude: a perspective on Its potential role in mortality in viral pneumonia-associated ARDS and implications for personalized critical care.Critical care (London, England) · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aims to investigate the impact of high altitude (HA) hypoxia on ferroptosis in lung tissue and the evaluate the preventative effect of Dimethyl fumarate (DMF) on lung inflammation.
methodsProteomic analysis was performed in plasma of volunteers ascending to high altitude, lung tissue of ALI rats, co-cultured lung epithelial (BEAS-2B cells) and macrophages (THP-1 cells) under hypoxia, either individually or in co-culture setting. DMF was pre-treated with rats or BEAS-2B cells before ferroptosis indexes and inflammatory cytokines were determined. Knock-down or overexpression of SLC7A11 in BEAS-2B cell was performed to further verify the role of DMF in alleviating ferroptosis and inflammation in ALI.
resultsProteomic analysis of human plasma, rat lung tissue and lung epithelial cells identified Differentially expressed proteins (DEPs) enriched in the ferroptosis. HA exposure increased inflammatory response and lung injury, which could be alleviated by DMF. Co-culture of two cell types lead to a more pronounced ferroptotic response in BEAS-2B cells and an elevated level of cytokine expression in THP-1 cells under hypoxia condition, which could also be ameliorated by DMF. Knockdown of SLC7A11 results in a reversal of ferroptosis and macrophage mediated inflammation, which were improved by increasing Nrf2 expression through DMF treatment.
conclusionThis study revealed that a reciprocal regulatory relationship between ferroptosis of lung epithelial cells and macrophage-mediated inflammation was one of the critical mechanisms contributing to HA exposure triggered ALI. Furthermore, DMF could alleviates hypoxia induced ALI by upregulating Nrf2/SLC7A11 pathway, making it a potential protective agent against HA hypoxia induced ALI.
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