<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Brazovskaja A</submitter><funding>Swiss National Science Foundation</funding><funding>European Research Council</funding><pagination>5827</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11239663</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>The liver has the remarkable capacity to regenerate. In the clinic, regeneration is induced by portal vein embolization, which redirects portal blood flow, resulting in liver hypertrophy in locations with increased blood supply, and atrophy of embolized segments. Here, we apply single-cell and single-nucleus transcriptomics on healthy, hypertrophied, and atrophied patient-derived liver samples to explore cell states in the regenerating liver. Our data unveils pervasive upregulation of genes associated with developmental processes, cellular adhesion, and inflammation in post-portal vein embolization liver, disrupted portal-central hepatocyte zonation, and altered cell subtype composition of endothelial and immune cells. Interlineage crosstalk analysis reveals mesenchymal cells as an interac</pubmed_abstract><journal>Nature communications</journal><pubmed_title>Cell atlas of the regenerating human liver after portal vein embolization.</pubmed_title><pmcid>PMC11239663</pmcid><funding_grant_id>310030_192604</funding_grant_id><funding_grant_id>758877</funding_grant_id><funding_grant_id>192604</funding_grant_id><funding_grant_id>874606</funding_grant_id><funding_grant_id>Organomics-758877</funding_grant_id><funding_grant_id>310030</funding_grant_id><funding_grant_id>803441</funding_grant_id><funding_grant_id>Braintime-874606</funding_grant_id><pubmed_authors>Treutlein B</pubmed_authors><pubmed_authors>Korner C</pubmed_authors><pubmed_authors>Brosch M</pubmed_authors><pubmed_authors>Camp JG</pubmed_authors><pubmed_authors>Hampe J</pubmed_authors><pubmed_authors>Denecke T</pubmed_authors><pubmed_authors>Holtackers R</pubmed_authors><pubmed_authors>Santel M</pubmed_authors><pubmed_authors>Schaffer T</pubmed_authors><pubmed_authors>Gomes T</pubmed_authors><pubmed_authors>Eckel JC</pubmed_authors><pubmed_authors>He Z</pubmed_authors><pubmed_authors>Dannemann M</pubmed_authors><pubmed_authors>Wahle P</pubmed_authors><pubmed_authors>Damm G</pubmed_authors><pubmed_authors>Seehofer D</pubmed_authors><pubmed_authors>Brazovskaja A</pubmed_authors><pubmed_authors>Hansel R</pubmed_authors><pubmed_authors>Seimiya M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cell atlas of the regenerating human liver after portal vein embolization.</name><description>The liver has the remarkable capacity to regenerate. In the clinic, regeneration is induced by portal vein embolization, which redirects portal blood flow, resulting in liver hypertrophy in locations with increased blood supply, and atrophy of embolized segments. Here, we apply single-cell and single-nucleus transcriptomics on healthy, hypertrophied, and atrophied patient-derived liver samples to explore cell states in the regenerating liver. Our data unveils pervasive upregulation of genes associated with developmental processes, cellular adhesion, and inflammation in post-portal vein embolization liver, disrupted portal-central hepatocyte zonation, and altered cell subtype composition of endothelial and immune cells. Interlineage crosstalk analysis reveals mesenchymal cells as an interac</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2025-04-05T15:49:36.814Z</modification><creation>2025-04-05T15:49:36.814Z</creation></dates><accession>S-EPMC11239663</accession><cross_references><pubmed>38992008</pubmed><doi>10.1038/s41467-024-49236-7</doi></cross_references></HashMap>