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Mature Polarized Hepatocyte Organoids Derived from Human Embryonic Stem Cells for Modeling the Pathogenesis and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease and Therapeutic Drug Screening

GSE303090 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/01/28 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 12 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
12 samples: 3 × P-hep-orgs, Control, Day2, vs 3 × P-hep-orgs, FFAs, Day2, vs 3 × P-hep-orgs, Control, Day10, vs 3 × P-hep-orgs, FFAs, Day10,Groups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Modeling pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease and therapeutic drug screening using hESC-derived mature polarized hepatocyte organoidsStem cell research & therapy · 2025
Summary (written by the submitters)
Metabolic dysfunction-associated steatotic liver disease (MASLD), the most prevalent chronic liver disorder worldwide, exhibits complex pathogenesis and lacks effective targeted therapeutics. Existing animal models are limited by prolonged induction periods and interspecies discrepancies, while conventional monolayer hepatocyte cultures fail to recapitulate disease pathology due to inadequate polarization and functional immaturity.
Read the full summary ↓
To overcome these constraints, this study established an in vitro MASLD model using human-derived mature polarized hepatocyte organoids (P-hep-orgs). P-hep-orgs were generated through directed differentiation of human embryonic stem cells (hESCs), with their structural and functional maturity validated by sequential expression analysis of stage-specific markers (OCT4, SOX17, ALB) and polarized localization of tight junction protein ZO-1 and multidrug resistance protein MDR1. Subsequent treatment with 450 μM free fatty acids (FFAs) induced key pathological features including lipid accumulation, oxidative stress, and disruption of polarized architecture. Dynamic disease progression was modeled through time-dependent interventions: short-term exposure (1-2 days) elicited early-stage phenotypes (e.g., extensive lipid droplet deposition, elevated triglycerides and supernatant glucose, increased reactive oxygen species, upregulation of pro-apoptotic genes), whereas prolonged treatment (≥10 days) recapitulated advanced manifestations (cholesterol accumulation, enhanced apoptosis, loss of polarization, and ductular reaction). Transcriptomic profiling demonstrated high similarity between this model and metabolic dysfunction-associated steatohepatitis (MASH) patient livers, revealing conserved mechanisms of glucolipid metabolic dysregulation, inflammation, and fibrotic pathway activation. Pharmacological validation confirmed that vitamin E, ursodeoxycholic acid, and empagliflozin significantly ameliorated lipid deposition, suppressed ROS generation, and restored albumin secretion. The model enables disease induction and drug evaluation within two weeks, substantially shortening the timeline compared to animal models, while its human origin eliminates species-specific drug response biases. This P-heporg-based MASLD platform provides an efficient and physiologically relevant foundation for investigating disease mechanisms and accelerating anti-MASLD drug discovery. Future integration of non-parenchymal cells will further enhance microenvironmental fidelity.
Published in
Modeling pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease and therapeutic drug screening using hESC-derived mature polarized hepatocyte organoids
Qin C, Wu H, Liao P et al. · Stem cell research & therapy 2025 · PMID 41422067 · doi:10.1186/s13287-025-04865-7
This dataset
Open GSE303090 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE303090_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1294139 and SRA study SRP602341. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41422067) ↗
Study design
3 × P-hep-orgs, Control, Day2, vs 3 × P-hep-orgs, FFAs, Day2, vs 3 × P-hep-orgs, Control, Day10, vs 3 × P-hep-orgs, FFAs, Day10,

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.