<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tao M</submitter><funding>Hubei Province Natural Science Foundation</funding><funding>National Natural Science Foundation of China</funding><pagination>593-608</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12869262</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>80</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Abnormalities in inflammation resolution function are intimately linked to chronic inflammation, and proresolution therapies may offer novel opportunities for IBD treatment. Developmental endothelial locus 1 (DEL-1), a natural modulator of tissue immunity and inflammation resolution, has not been studied in IBD.&lt;h4>Objectives&lt;/h4>We aimed to investigate the expression and functions of DEL-1 in IBD.&lt;h4>Methods&lt;/h4>Assessment of DEL-1 expression in patients, murine models, and cellular levels. To explore the effects of DEL-1 in the acute and recovery phases of inflammation, overexpression plasmids, adeno-associated viruses for DEL-1 knockdown, and DEL-1-Fc fusion proteins were administered to cells and mice. Additionally, the potential mechanism of DEL-1 in IBD was demon</pubmed_abstract><journal>Journal of advanced research</journal><pubmed_title>Developmentally endothelial locus-1 facilitates intestinal inflammation resolution by suppressing the Cmpk2-cGAS-STING pathway and promoting reparatory macrophage transition.</pubmed_title><pmcid>PMC12869262</pmcid><funding_grant_id>82270559</funding_grant_id><funding_grant_id>82273321</funding_grant_id><funding_grant_id>81770554</funding_grant_id><funding_grant_id>81974383</funding_grant_id><funding_grant_id>2023AFD044</funding_grant_id><funding_grant_id>82070572</funding_grant_id><pubmed_authors>Tao M</pubmed_authors><pubmed_authors>Tang M</pubmed_authors><pubmed_authors>Lin R</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Fu Y</pubmed_authors><pubmed_authors>Chen C</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Yan W</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Zhao X</pubmed_authors><pubmed_authors>Feng Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Developmentally endothelial locus-1 facilitates intestinal inflammation resolution by suppressing the Cmpk2-cGAS-STING pathway and promoting reparatory macrophage transition.</name><description>&lt;h4>Introduction&lt;/h4>Abnormalities in inflammation resolution function are intimately linked to chronic inflammation, and proresolution therapies may offer novel opportunities for IBD treatment. Developmental endothelial locus 1 (DEL-1), a natural modulator of tissue immunity and inflammation resolution, has not been studied in IBD.&lt;h4>Objectives&lt;/h4>We aimed to investigate the expression and functions of DEL-1 in IBD.&lt;h4>Methods&lt;/h4>Assessment of DEL-1 expression in patients, murine models, and cellular levels. To explore the effects of DEL-1 in the acute and recovery phases of inflammation, overexpression plasmids, adeno-associated viruses for DEL-1 knockdown, and DEL-1-Fc fusion proteins were administered to cells and mice. Additionally, the potential mechanism of DEL-1 in IBD was demon</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-15T12:08:12.951Z</modification><creation>2026-07-04T03:12:44.859Z</creation></dates><accession>S-EPMC12869262</accession><cross_references><pubmed>40288675</pubmed><doi>10.1016/j.jare.2025.04.030</doi></cross_references></HashMap>