<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Liu W</submitter><funding>National Natural Science Foundation of China</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>Sepsis-induced cardiomyopathy (&lt;i>SIC&lt;/i>) 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 &lt;i>SIC&lt;/i> based on clinical and laboratory evidence.&lt;h4>Methods&lt;/h4>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</pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>1009726</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9676239</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction.</pubmed_title><pmcid>PMC9676239</pmcid><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Guo X</pubmed_authors><pubmed_authors>Hong T</pubmed_authors><pubmed_authors>Shen Y</pubmed_authors><pubmed_authors>He B</pubmed_authors><pubmed_authors>Zhang Q</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Jin L</pubmed_authors><pubmed_authors>Su F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction.</name><description>&lt;h4>Background&lt;/h4>Sepsis-induced cardiomyopathy (&lt;i>SIC&lt;/i>) 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 &lt;i>SIC&lt;/i> based on clinical and laboratory evidence.&lt;h4>Methods&lt;/h4>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</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-07-14T17:36:53.298Z</modification><creation>2025-04-19T14:44:15.395Z</creation></dates><accession>S-EPMC9676239</accession><cross_references><pubmed>36419491</pubmed><doi>10.3389/fcvm.2022.1009726</doi></cross_references></HashMap>