{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pita-Juarez Y"],"funding":["Office of Research Infrastructure Programs, National Institutes of Health","NIDDK NIH HHS","National Blood Clot Alliance","U.S. Food and Drug Administration","NCI NIH HHS","NIH Support Grant","Gates Foundation"],"pagination":["56"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11907808"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(1)"],"pubmed_abstract":["<h4>Background</h4>The molecular underpinnings of organ dysfunction in severe COVID-19 and its potential long-term sequelae are under intense investigation. To shed light on these in the context of liver function, we perform single-nucleus RNA-seq and spatial transcriptomic profiling of livers from 17 COVID-19 decedents.<h4>Results</h4>We identify hepatocytes positive for SARS-CoV-2 RNA with an expression phenotype resembling infected lung epithelial cells, and a central role in a pro-fibrotic TGFβ signaling cell-cell communications network. Integrated analysis and comparisons with healthy controls reveal extensive changes in the cellular composition and expression states in COVID-19 liver, providing the underpinning of hepatocellular injury, ductular reaction, pathologic vascular expansio"],"journal":["Genome biology"],"pubmed_title":["A single-nucleus and spatial transcriptomic atlas of the COVID-19 liver reveals topological, functional, and regenerative organ disruption in patients."],"pmcid":["PMC11907808"],"funding_grant_id":["S10RR027050","PR200524P1","P30CA013696","R01 CA258776","R01 HL129506-07","R37CA258829","HHSF223201810172C","INV-027498","P30 DK046200","U54CA225088","R21CA263381","P30 DK135043","Massachusetts Life Sciences Center","K08CA222663"],"pubmed_authors":["Phelan S","Myloserdnyy A","Liang Y","Ashenberg O","Warren S","Patrick M","Zhang S","Rane T","Subramanian A","Sturm A","Tsai LT","Essene AL","Huang P","Izar B","Villani AC","Jiang ZG","Hibshoosh H","Slyper M","Chen R","Hecht J","Rozenblatt-Rosen O","Pita-Juarez Y","Niezen S","Wardhani A","Kramer Z","Melms JC","Beechem J","Tran VM","He S","Delorey TM","Szabo G","Karagkouni D","Biermann J","Jacobs C","Brook OR","Padera RF","MacParland SA","Popov YV","Riedel S","Yalcin Y","Hide W","Hung D","Fleming SJ","Vlachos IS","Bader GD","Bloom-Ackermann Z","Babadi M","Phillips D","Miller E","Porter CBM","Amin AD","Ziegler CGK","Reeves J","Nam A","Imad N","Solomon IH","Gomez J","Pant D","Regev A","Shalek AK","Hether T","Naderi P","Skelton-Badlani D","Pan L","Kalavros N","Andrews TS","Gregory M","Veregge M"],"additional_accession":[]},"is_claimable":false,"name":"A single-nucleus and spatial transcriptomic atlas of the COVID-19 liver reveals topological, functional, and regenerative organ disruption in patients.","description":"<h4>Background</h4>The molecular underpinnings of organ dysfunction in severe COVID-19 and its potential long-term sequelae are under intense investigation. To shed light on these in the context of liver function, we perform single-nucleus RNA-seq and spatial transcriptomic profiling of livers from 17 COVID-19 decedents.<h4>Results</h4>We identify hepatocytes positive for SARS-CoV-2 RNA with an expression phenotype resembling infected lung epithelial cells, and a central role in a pro-fibrotic TGFβ signaling cell-cell communications network. Integrated analysis and comparisons with healthy controls reveal extensive changes in the cellular composition and expression states in COVID-19 liver, providing the underpinning of hepatocellular injury, ductular reaction, pathologic vascular expansio","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-01T22:54:27.831Z","creation":"2025-04-06T10:47:51.989Z"},"accession":"S-EPMC11907808","cross_references":{"pubmed":["40087773"],"doi":["10.1186/s13059-025-03499-5"]}}