<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shi Y</submitter><funding>Science and Technology Bureau of Jiaxing City</funding><funding>Natural Science Foundation of Zhejiang Province</funding><funding>Zhejiang Provincial Health Bureau Science Foundation</funding><funding>Medical Science and technology development Foundation，Nanjing Department of Health</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Research and Development Program of China</funding><funding>Natural Science Foundation of Jiangsu Province</funding><pagination>e70315</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12034574</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(5)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Septic cardiomyopathy is a frequent complication in patients with sepsis and is associated with a high mortality rate. Given its clinical significance, understanding the precise underlying mechanism is of great value.&lt;h4>Methods and results&lt;/h4>Our results unveiled that Z-DNA binding protein 1 (ZBP1) is upregulated in myocardial tissues of lipopolysaccharide (LPS)-treated mice. Single-cell mRNA sequencing (scRNA-seq) and single-nucleus mRNA sequencing (snRNA-seq) indicated that Zbp1 mRNA in endothelial cells, fibroblasts and macrophages appeared to be elevated by LPS, which is partially consistent with the results of immunofluorescence. Through echocardiography, we identified that global deletion of ZBP1 improves cardiac dysfunction and the survival rate of LPS-treated m</pubmed_abstract><journal>Clinical and translational medicine</journal><pubmed_title>Myeloid deficiency of Z-DNA binding protein 1 restricts septic cardiomyopathy via promoting macrophage polarisation towards the M2-subtype.</pubmed_title><pmcid>PMC12034574</pmcid><funding_grant_id>82400319</funding_grant_id><funding_grant_id>2023AZ31003</funding_grant_id><funding_grant_id>YKK24067</funding_grant_id><funding_grant_id>2024KY442</funding_grant_id><funding_grant_id>BK20240226</funding_grant_id><funding_grant_id>2022YFA1205904</funding_grant_id><funding_grant_id>ZCLMS25H1503</funding_grant_id><funding_grant_id>82470384</funding_grant_id><pubmed_authors>Ni J</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>He L</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Shi Y</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Tan X</pubmed_authors><pubmed_authors>Xu B</pubmed_authors><pubmed_authors>Sun S</pubmed_authors><pubmed_authors>Han J</pubmed_authors><pubmed_authors>Xu X</pubmed_authors><pubmed_authors>Yu X</pubmed_authors><pubmed_authors>Kang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myeloid deficiency of Z-DNA binding protein 1 restricts septic cardiomyopathy via promoting macrophage polarisation towards the M2-subtype.</name><description>&lt;h4>Background&lt;/h4>Septic cardiomyopathy is a frequent complication in patients with sepsis and is associated with a high mortality rate. Given its clinical significance, understanding the precise underlying mechanism is of great value.&lt;h4>Methods and results&lt;/h4>Our results unveiled that Z-DNA binding protein 1 (ZBP1) is upregulated in myocardial tissues of lipopolysaccharide (LPS)-treated mice. Single-cell mRNA sequencing (scRNA-seq) and single-nucleus mRNA sequencing (snRNA-seq) indicated that Zbp1 mRNA in endothelial cells, fibroblasts and macrophages appeared to be elevated by LPS, which is partially consistent with the results of immunofluorescence. Through echocardiography, we identified that global deletion of ZBP1 improves cardiac dysfunction and the survival rate of LPS-treated m</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 May</publication><modification>2026-06-01T14:51:52.128Z</modification><creation>2025-07-06T03:05:34.788Z</creation></dates><accession>S-EPMC12034574</accession><cross_references><pubmed>40289345</pubmed><doi>10.1002/ctm2.70315</doi></cross_references></HashMap>