Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction

Abstract

The level of LCN-2 is significantly increased in <i>SIC</i> at both circulating and tissue levels, which is correlated with the severity of myocardial injury indicators, and may work as an early and great predictor of <i>SIC</i>. LCN-2 probably participates in the process of septic myocardial injury through mediating lipid accumulation and affecting mitochondrial function.