ArticleInflammation2025
Targeting Lcn2 to Inhibit Myocardial Cell Ferroptosis is a Potential Therapy for Alleviating Septic Cardiomyopathy.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Exploring the Role of the LCN2-DHODH Interaction in Mitochondrial Ferroptosis During Sepsis-Induced Myocardial Injury and LPS-Induced HL-1 Cardiomyocyte Injury.International journal of molecular sciences · 2026Article
- Inhibition of iron overload and ferroptosis attenuates sepsis-induced myocardial injury in mice through STAT3/Lcn2 pathway.Journal of cardiothoracic surgery · 2026Article
- Lipocalin 2: a double-edged sword in cellular ferroptosis.Cell biology and toxicology · 2026Review
- Article
- Emerging roles of lipocalin-2-mediated neuroimmune interactions in chronic pain and itch.Frontiers in pharmacology · 2026Review
- Isoflurane and Surgical Stress Disrupt Fatty Acid and Carbon Metabolism Leading to Cardiomyopathy.bioRxiv : the preprint server for biology · 2025Article
- Lipocalin-2-mediated ferroptosis as a target for protection against light-induced photoreceptor degeneration.Molecular medicine (Cambridge, Mass.) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Septic cardiomyopathy (SCM) represents a key feature of sepsis-associated cardiovascular failure, and ferroptosis is one of the essential causes of septic cardiac dysfunction. In this study, combined with omics analysis and in vivo experiments, we verified the damage of ferroptosis on cardiac tissue in septic mice and mined the target genes that can inhibit ferroptosis in cardiomyocytes. Lipocalin-2 (Lcn2) was identified to be associated with SCM progression via integrated transcriptomic and proteomic analyses. Sepsis was induced by cecal ligation and perforation (CLP) in mice. Ferroptosis and cardiac dysfunction were detected by pathological tissue staining and ELISA. However, after the knockout of Lcn2, cardiomyocyte ferroptosis was significantly suppressed, inflammatory infiltrates were reduced, reactive oxygen species (ROS) levels were lowered, mitochondrial damage was alleviated, and cardiac function was restored in CLP mice. In summary, this study found that Lcn2 can be a potential target for inhibiting ferroptosis in SCM. Targeting Lcn2 can effectively inhibit inflammation, improve mitochondrial dysfunction, inhibit cardiomyocyte ferroptosis, and alleviate SCM.
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Registered trials
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