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

ABSTRACT:

Background

Sepsis-induced cardiomyopathy (SIC) is one major cause of death for sepsis but lacks timely diagnosis and specific treatment due to unclear mechanisms. Lipocalin-2 (LCN-2) is a key regulator of lipid metabolism which has been recently proved closely related to sepsis, however, the relationship between LCN-2 and septic myocardial injury remains unknown. We aim to explore the role of LCN-2 in the pathological progress of SIC based on clinical and laboratory evidence.

Methods

Consecutive patients admitted to the intensive care unit (ICU) from August 2021 to April 2022 fulfilling the criteria of severe sepsis were included. The level of LCN-2 in plasma was assayed and analyzed with clinical characteristics. Biostatistical analysis was performed for furth

SUBMITTER: Liu W 

PROVIDER: S-EPMC9676239 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature