<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gonzalez-Acera M</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>European Research Council</funding><funding>Volkswagen Foundation</funding><funding>Interdisciplinary Centre for Clinical Research</funding><pagination>1602-1615</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12505074</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>74(10)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>IBD is a chronic inflammatory condition driven by complex genetic and immune interactions, yet preclinical models often fail to fully recapitulate all aspects of the human disease. A systematic comparison of commonly used IBD models is essential to identify conserved molecular mechanisms and improve translational relevance.&lt;h4>Objective&lt;/h4>We performed a multimodel transcriptomic analysis of 13 widely used IBD mouse models to uncover coregulatory gene networks conserved between preclinical colitis/ileitis and human IBD and to define model-specific and conserved cellular, subcellular and molecular signatures.&lt;h4>Design&lt;/h4>We employed comparative transcriptomic analyses with curated and a priori statistical correlative methods between mouse models versus IBD patient data</pubmed_abstract><journal>Gut</journal><pubmed_title>Integrated multimodel analysis of intestinal inflammation exposes key molecular features of preclinical and clinical IBD.</pubmed_title><pmcid>PMC12505074</pmcid><funding_grant_id>CRU 5023 (project number 50474582)</funding_grant_id><funding_grant_id>531560612</funding_grant_id><funding_grant_id>536563567</funding_grant_id><funding_grant_id>StG “iMOTIONS” 101078069</funding_grant_id><funding_grant_id>418055832</funding_grant_id><funding_grant_id>CRC 1340-B06 (project number 372486779)</funding_grant_id><funding_grant_id>TRR241 375876048 (A03, A05, A08, B05, Z03)</funding_grant_id><funding_grant_id>101078069</funding_grant_id><funding_grant_id>A76, A93, J96, and ELAN P120</funding_grant_id><funding_grant_id>510624836</funding_grant_id><funding_grant_id>KFO5024 505539112 (Project- A3)</funding_grant_id><funding_grant_id>CRC 1449-B04 and Z02 (project number 431232613)</funding_grant_id><funding_grant_id>SFB1181 (C05)</funding_grant_id><funding_grant_id>INST 335/597-1</funding_grant_id><pubmed_authors>Bacher P</pubmed_authors><pubmed_authors>Sanders AD</pubmed_authors><pubmed_authors>Bojarski C</pubmed_authors><pubmed_authors>Schurmann S</pubmed_authors><pubmed_authors>Gunther C</pubmed_authors><pubmed_authors>Sturm G</pubmed_authors><pubmed_authors>Stolzer I</pubmed_authors><pubmed_authors>Gießl A</pubmed_authors><pubmed_authors>Lopez-Posadas R</pubmed_authors><pubmed_authors>Wang R</pubmed_authors><pubmed_authors>Triantafyllopoulou A</pubmed_authors><pubmed_authors>Bao LL</pubmed_authors><pubmed_authors>Mascia F</pubmed_authors><pubmed_authors>Krug SM</pubmed_authors><pubmed_authors>Koop K</pubmed_authors><pubmed_authors>Gamez-Belmonte R</pubmed_authors><pubmed_authors>Gupta P</pubmed_authors><pubmed_authors>Wirtz S</pubmed_authors><pubmed_authors>Leppkes M</pubmed_authors><pubmed_authors>Neufert C</pubmed_authors><pubmed_authors>Klose CSN</pubmed_authors><pubmed_authors>Schickedanz L</pubmed_authors><pubmed_authors>Limberger H</pubmed_authors><pubmed_authors>Patankar JV</pubmed_authors><pubmed_authors>Dinkel M</pubmed_authors><pubmed_authors>Bubeck M</pubmed_authors><pubmed_authors>Naschberger E</pubmed_authors><pubmed_authors>Atreya I</pubmed_authors><pubmed_authors>Schumann M</pubmed_authors><pubmed_authors>Diemand L</pubmed_authors><pubmed_authors>Plattner C</pubmed_authors><pubmed_authors>TRR241 IBDome Consortium</pubmed_authors><pubmed_authors>Erkert L</pubmed_authors><pubmed_authors>Sturzl M</pubmed_authors><pubmed_authors>Romagnani C</pubmed_authors><pubmed_authors>Trajanoski Z</pubmed_authors><pubmed_authors>Diefenbach A</pubmed_authors><pubmed_authors>Pruß MS</pubmed_authors><pubmed_authors>Atreya R</pubmed_authors><pubmed_authors>Hildner K</pubmed_authors><pubmed_authors>Neurath MF</pubmed_authors><pubmed_authors>Gerlach K</pubmed_authors><pubmed_authors>Gonzalez-Acera M</pubmed_authors><pubmed_authors>Cineus R</pubmed_authors><pubmed_authors>Britzen-Laurent N</pubmed_authors><pubmed_authors>Voskens C</pubmed_authors><pubmed_authors>Radbruch A</pubmed_authors><pubmed_authors>Siegmund B</pubmed_authors><pubmed_authors>Leupold T</pubmed_authors><pubmed_authors>Schulzke JD</pubmed_authors><pubmed_authors>Waldner M</pubmed_authors><pubmed_authors>Scheffold A</pubmed_authors><pubmed_authors>Ronchi F</pubmed_authors><pubmed_authors>Kuhl AA</pubmed_authors><pubmed_authors>Zundler S</pubmed_authors><pubmed_authors>Hegazy AN</pubmed_authors><pubmed_authors>Ludwig LS</pubmed_authors><pubmed_authors>Becker C</pubmed_authors><pubmed_authors>Chang HD</pubmed_authors><pubmed_authors>Weidinger C</pubmed_authors><pubmed_authors>Weigmann B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Integrated multimodel analysis of intestinal inflammation exposes key molecular features of preclinical and clinical IBD.</name><description>&lt;h4>Background&lt;/h4>IBD is a chronic inflammatory condition driven by complex genetic and immune interactions, yet preclinical models often fail to fully recapitulate all aspects of the human disease. A systematic comparison of commonly used IBD models is essential to identify conserved molecular mechanisms and improve translational relevance.&lt;h4>Objective&lt;/h4>We performed a multimodel transcriptomic analysis of 13 widely used IBD mouse models to uncover coregulatory gene networks conserved between preclinical colitis/ileitis and human IBD and to define model-specific and conserved cellular, subcellular and molecular signatures.&lt;h4>Design&lt;/h4>We employed comparative transcriptomic analyses with curated and a priori statistical correlative methods between mouse models versus IBD patient data</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-07-15T07:35:50.998Z</modification><creation>2026-07-01T03:07:19.473Z</creation></dates><accession>S-EPMC12505074</accession><cross_references><pubmed>40301114</pubmed><doi>10.1136/gutjnl-2024-333729</doi></cross_references></HashMap>