<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(5)</volume><submitter>Li Y</submitter><pubmed_abstract>Myocardial injury is a serious complication of sepsis. The present study aimed to identify potential biomarkers of sepsis-induced myocardial injury. Differentially expressed genes (DEGs) in patients and mice with sepsis-induced myocardial injury were identified via bioinformatic analysis. The identified DEG was tested in elderly patients with sepsis-induced myocardial injury. We identified 19 co-expressed DEGs. The most significant DEG was eotaxin-1/CCL11. We enrolled 25 controls without infections and 28 patients with sepsis-induced myocardial injury. Six of patients died within 30 days. Circulating eotaxin-1/CCL11 levels were significantly higher in patients with sepsis-induced myocardial injury than controls and were higher in non-survivors than survivors (both P &lt; 0.01). Eotaxin-1/CCL11 was positively correlated with troponin I (r=0.48, P=0.01), B-type natriuretic peptide (BNP, r=0.44, P=0.02), and white blood cell (WBC) count (r=0.41, P=0.03). For the prediction of 30-day mortality, eotaxin-1/CCL11 had the greatest discriminatory ability (AUC 0.97) compared with troponin I (AUC 0.89), BNP (AUC 0.80), and WBC count (AUC 0.86). Taken together, eotaxin-1/CCL11 was upregulated in sepsis-injured myocardium and circulating eotaxin-1/CCL11 was a biomarker for predicting severity and mortality of elderly patients with sepsis-induced myocardial injury. These results suggest that eotaxin-1/CCL11 may become a useful biomarkers and potential therapeutic target for sepsis-induced myocardial injury.</pubmed_abstract><journal>Aging</journal><pagination>4463-4473</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7093174</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Role of eotaxin-1/CCL11 in sepsis-induced myocardial injury in elderly patients.</pubmed_title><pmcid>PMC7093174</pmcid><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Qiu C</pubmed_authors><pubmed_authors>Liao G</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Zhang R</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors><pubmed_authors>Zhang Q</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of eotaxin-1/CCL11 in sepsis-induced myocardial injury in elderly patients.</name><description>Myocardial injury is a serious complication of sepsis. The present study aimed to identify potential biomarkers of sepsis-induced myocardial injury. Differentially expressed genes (DEGs) in patients and mice with sepsis-induced myocardial injury were identified via bioinformatic analysis. The identified DEG was tested in elderly patients with sepsis-induced myocardial injury. We identified 19 co-expressed DEGs. The most significant DEG was eotaxin-1/CCL11. We enrolled 25 controls without infections and 28 patients with sepsis-induced myocardial injury. Six of patients died within 30 days. Circulating eotaxin-1/CCL11 levels were significantly higher in patients with sepsis-induced myocardial injury than controls and were higher in non-survivors than survivors (both P &lt; 0.01). Eotaxin-1/CCL11 was positively correlated with troponin I (r=0.48, P=0.01), B-type natriuretic peptide (BNP, r=0.44, P=0.02), and white blood cell (WBC) count (r=0.41, P=0.03). For the prediction of 30-day mortality, eotaxin-1/CCL11 had the greatest discriminatory ability (AUC 0.97) compared with troponin I (AUC 0.89), BNP (AUC 0.80), and WBC count (AUC 0.86). Taken together, eotaxin-1/CCL11 was upregulated in sepsis-injured myocardium and circulating eotaxin-1/CCL11 was a biomarker for predicting severity and mortality of elderly patients with sepsis-induced myocardial injury. These results suggest that eotaxin-1/CCL11 may become a useful biomarkers and potential therapeutic target for sepsis-induced myocardial injury.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2020-05-22T14:44:25Z</modification><creation>2020-05-22T14:44:25Z</creation></dates><accession>S-EPMC7093174</accession><cross_references><pubmed>32147601</pubmed><doi>10.18632/aging.102896 </doi></cross_references></HashMap>