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Single-cell fixed RNAseq of liver fibrosis progression and regression

GSE295293 Mus musculus (mouse) Single-cell RNA-seq 9 samples Submitted 2026/03/27 Platform GPL28457
At a glance

Single-cell RNA-seq · mouse · 9 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism
Mus musculus (mouse)
Samples
9 samples: 3 × control livers, nontreated vs 3 × fibrosis livers, thioacetamide treated vs 3 × fibrosis livers, thioacetamide treated, regression 2 weeksGroups 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.
Summary (written by the submitters)
Liver fibrosis regression is a dynamic process involving a variety of hepatic and immune cell populations. Using single-cell fixed RNA profiling (FLEX) on mouse livers from control, TAA-induced cirrhotic, and regression phases, we analyzed 38,136 cells across 10 major cell types. Regression was characterized by the emergence of pericentral hepatocytes enriched in detoxification and antioxidant genes (e.g., Cyp2e1, Txn1), which secreted RARRES2 to modulate hepatic stellate cells (HSCs).
Read the full summary ↓
Recovered liver sinusoidal endothelial cells (LSECs) expressed scar-resolving genes (Mmp14, Ctsl) and restored fenestrae structure. Kupffer cells regained anti-inflammatory phenotypes, while SEMA4D, produced by monocyte-derived macrophages, activated HSCs; blockade of SEMA4D reduced fibrosis in vivo. Fibrogenic cholangiocyte subsets and LMCD1⁺ HSCs were diminished during regression, with LMCD1 identified as a novel marker of HSC activation. Additionally, NK/T cells, B cells, and neutrophils displayed recovery-associated transcriptional signatures. This single-cell atlas uncovers key transcriptional programs and intercellular interactions driving fibrosis resolution and highlights potential therapeutic targets for chronic liver disease.
This dataset
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.

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 GSE295293_RAW.tar (it can run to tens of gigabytes).

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.

What the files usually look like: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1254133 and SRA study SRP580456. Searching any of these in the dataset finder brings you back here.

Study design
3 × control livers, nontreated vs 3 × fibrosis livers, thioacetamide treated vs 3 × fibrosis livers, thioacetamide treated, regression 2 weeks

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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
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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.