ArticleNature genetics2024
A spatiotemporal atlas of cholestatic injury and repair in mice.
Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- TGF-β serves as a critical signaling determinant of liver progenitor cell activation and function.The Journal of clinical investigation · 2026Article
- Spatial hepatology: Decoding liver zonation for metabolic and regenerative therapeutics (Review).International journal of molecular medicine · 2026Review
- The hepatic portal area in homeostasis and disease.Clinical and molecular hepatology · 2026Article
- A subset of hepatic fibroblasts marked by Gli1 expression generates portal fibrosis and promotes ductular reaction.JHEP reports : innovation in hepatology · 2026Article
- SAA/FPR2 Signaling Between Pericentral Hepatocytes and Macrophages Exacerbates Zonated Liver Transplant Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- SOFisher: reinforcement learning-guided experiment designs for spatial omics.Nature communications · 2026Article
- Review
- Single-nucleus chromatin landscapes of cholestatic injury and repair in mice liver.Scientific data · 2026Article
- Spatiotemporal Transcriptomics Characterizes Immune Microenvironment During Mouse Liver Aging.Aging cell · 2026Article
- Clec3b⁺ fibroblasts are the primary effectors of portal fibrosis following activation via a KLF4/periostin axis.Nature communications · 2026Article
- Targeting FGG alleviates cholestatic fibrosis by inhibiting hepatic stellate cell activation and regulating macrophage homeostasis.Journal of nanobiotechnology · 2026Article
- An immunobiliary single-cell atlas resolves crosstalk between type 2 conventional dendritic cells and γδ T cells in cholangitis.Nature communications · 2026Article
- Scalable discovery of spatial multicellular patterns via neighborhood-to-sequence transformation.Communications biology · 2026Article
- Conversion of Transplanted Mature Hepatocytes into AfpAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hepatocyte Mettl3 Deficiency Drives Primary Sclerosing Cholangitis and Liver Fibrosis via Cholangiocyte-Macrophage Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of aryl hydrocarbon receptor alleviates cholestatic liver injury by inhibiting inflammation.Cell communication and signaling : CCS · 2026Article
- MicroRNA signatures in inflammatory dental tissues: biomarkers and molecular mechanisms.Frontiers in molecular biosciences · 2026Review
- Massive hepatic necrosis-associated acute liver failure.eGastroenterology · 2026Review
Corrections and comments
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Authors and funding
31 authors at 6 institutions in 1 country.
Funding
Abstract
Cholestatic liver injuries, characterized by regional damage around the bile ductular region, lack curative therapies and cause considerable mortality. Here we generated a high-definition spatiotemporal atlas of gene expression during cholestatic injury and repair in mice by integrating spatial enhanced resolution omics sequencing and single-cell transcriptomics. Spatiotemporal analyses revealed a key role of cholangiocyte-driven signaling correlating with the periportal damage-repair response. Cholangiocytes express genes related to recruitment and differentiation of lipid-associated macrophages, which generate feedback signals enhancing ductular reaction. Moreover, cholangiocytes express high TGFβ in association with the conversion of liver progenitor-like cells into cholangiocytes during injury and the dampened proliferation of periportal hepatocytes during recovery. Notably, Atoh8 restricts hepatocyte proliferation during 3,5-diethoxycarbonyl-1,4-dihydro-collidin damage and is quickly downregulated after injury withdrawal, allowing hepatocytes to respond to growth signals. Our findings lay a keystone for in-depth studies of cellular dynamics and molecular mechanisms of cholestatic injuries, which may further develop into therapies for cholangiopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.