ArticleCytoJournal2026
Transcription factor EGR1 orchestrates ferroptosis to mitigate sepsis-induced myocardial injury by enhancing ferroportin expression.
Article in CytoJournal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Objective: Myocardial injury is a devastating complication of sepsis and a leading cause of mortality in critically ill patients. This study aimed to investigate the role and underlying mechanisms of early growth response factor 1 (EGR1) in sepsis-induced myocardial injury (SIMI). Material and Methods: A rat model of SIMI was established using cecal ligation and puncture, and Results: Septic rats exhibited significant inflammation, myocardial injury, apoptosis, and oxidative stress. Transcriptome sequencing revealed that EGR1 expression was downregulated in the myocardium of septic rats and associated with the ferroptosis pathway. Dual-luciferase reporter gene assays confirmed that EGR1 is directly bound to and activates the FPN promoter. Conclusion: This study provides a novel finding that EGR1 plays a pivotal protective role in myocardial injury through the direct transcriptional activation of FPN. Mechanistically, EGR1 alleviates SIMI by transcriptionally activating the FPN/xCT/GPX4 axis, which leads to the suppression of ferroptosis and oxidative stress and the preservation of mitochondrial function.
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