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.
View Article and Find Full Text PDFKorean J Physiol Pharmacol
November 2024