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<p>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.</p>

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Targeting Lcn2 to Inhibit Myocardial Cell Ferroptosis is a Potential Therapy for Alleviating Septic Cardiomyopathy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月3日

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  • Cheng Jiang,
  • MingTong Hou,
  • Shougang Sun,
  • Gang Chen,
  • Feng Bai,
  • Shengbao Wang

摘要

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.