ArticleFrontiers in medicine2024
Identification and verification of disulfidptosis-related genes in sepsis-induced acute lung injury.
Article in Frontiers in medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mechanism of Action ofBiology · 2026Article
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Integrative single-cell and bulk transcriptomic analyses identify a microglia-associated NAGLU signature linked to disulfidptosis-associated transcriptional patterns after spinal cord injury.Frontiers in immunology · 2026Article
- Disulfidptosis-associated gene signatures in sepsis: a diagnostic model based on an LLM-assisted bioinformatics analysis.Health information science and systems · 2025Article
- Molecular mechanisms and potential implications of ferroptosis, cuproptosis, and disulfidptosis in septic lung injury.Frontiers in medicine · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis-induced acute lung injury (ALI) is a common and serious complication of sepsis that eventually progresses to life-threatening hypoxemia. Disulfidptosis is a newly discovered type of cell death associated with the pathogenesis of different diseases. This study investigated the potential association between sepsis-induced acute lung injury and disulfidptosis by bioinformatics analysis. Methods: In order to identify differentially expressed genes (DEGs) linked to sepsis, we screened appropriate data sets from the GEO database and carried out differential analysis. The key genes shared by DEGs and 39 disulfidptosis-related genes were identified: ACSL4 and MYL6 mRNA levels of key genes were detected in different datasets. We then used a series of bioinformatics analysis techniques, such as immune cell infiltration analysis, protein-protein interaction (PPI) network, genetic regulatory network, and receiver operating characteristic (ROC), to investigate the possible relationship between key genes and sepsis. Then, experimental verification was obtained for changes in key genes in sepsis-induced acute lung injury. Finally, to investigate the relationship between genetic variants of MYL6 or ACSL4 and sepsis, Mendelian randomization (MR) analysis was applied. Results: Two key genes were found in this investigation: myosin light chain 6 (MYL6) and Acyl-CoA synthetase long-chain family member 4 (ACSL4). We verified increased mRNA levels of key genes in training datasets. Immune cell infiltration analysis showed that key genes were associated with multiple immune cell levels. Building the PPI network between MYL6 and ACSL4 allowed us to determine that their related genes had distinct biological functions. The co-expression genes of key genes were involved in different genetic regulatory networks. In addition, both the training and validation datasets confirmed the diagnostic capabilities of key genes by using ROC curves. Additionally, both Conclusion: We have discovered and confirmed that the key genes ACSL4 and MYL6, which are linked to disulfidptosis in sepsis-induced acute lung injury, may be useful in the diagnosis and management of septic acute lung injury.
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