← BioTransfer GEO Dataset Finder
GEO series

CXCL6 exacerbates metabolic dysfunction-associated steatohepatitis by suppressing LPIN1-mediated fatty acid oxidation in hepatocytes

GSE325102 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/06/03 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
12 samples: 4 × Liver, HFD, Wildtype # vs 4 × Liver, MASH, Wildtype # vs 4 × Liver, MASH, Cxcl5 KO #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
CXCL6 exacerbates metabolic dysfunction-associated steatohepatitis by suppressing LPIN1-mediated fatty acid oxidation in hepatocytesInternational journal of biological sciences · 2026
Summary (written by the submitters)
Progression of hepatic steatosis to metabolic dysfunction-associated steatohepatitis (MASH) involves impaired fatty acid (FA) oxidation, which causes lipotoxicity and inflammation in hepatocytes. MASH is characterized by upregulation of the neutrophil-recruiting chemokine CXCL6. Although hepatocytes produce CXCL6, its direct contribution to MASH progression in hepatocytes, beyond neutrophil recruitment, remains unclear.
Read the full summary ↓
Here, we show that Cxcl5, the murine homolog of human CXCL6, promotes steatosis-to-MASH transition when overexpressed in the mouse liver, whereas Cxcl5 deficiency protects against diet-induced MASH. Transcriptomic analysis of Cxcl5-deficient mice showed upregulation of FA metabolism genes. This is accompanied by reduced hepatic FA levels and increased Lipin-1 (LPIN1) expression, which activates PPARα. In vitro, recombinant mouse CXCL5 suppressed LPIN1 and PPARα expression in mouse hepatocytes, whereas Cxcl5-deficient hepatocytes exhibited elevated levels of both. Mechanistically, CXCL6 induced JNK activation, leading to inhibitory phosphorylation of the glucocorticoid receptor (GR). Luciferase assays demonstrated that CXCL6 attenuated GR-dependent LPIN1 promoter activation. Lpin1 knockdown reversed the protective phenotype in Cxcl5-deficient mice, indicating that LPIN1 suppression is essential for CXCL6-driven MASH progression. Human MASH samples consistently exhibited reduced hepatic LPIN1 expression and an inverse correlation between LPIN1 and CXCL6 expression. In conclusion, CXCL6 drives MASH progression by inhibiting GR-mediated LPIN1 transactivation in hepatocytes, impairing FA oxidation and promoting lipotoxicity.
Published in
CXCL6 exacerbates metabolic dysfunction-associated steatohepatitis by suppressing LPIN1-mediated fatty acid oxidation in hepatocytes
Cho YE, Kim MJ, Kim Y et al. · International journal of biological sciences 2026 · PMID 42212316 · doi:10.7150/ijbs.129358
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 GSE325102_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: 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 PRJNA1438650 and SRA study SRP684489. Searching any of these in the dataset finder brings you back here.

Study design
4 × Liver, HFD, Wildtype # vs 4 × Liver, MASH, Wildtype # vs 4 × Liver, MASH, Cxcl5 KO #

Supports a between-group comparison across 12 samples.

How we read this: 3 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

Search all mouse RNA-seq datasets in GEO →

Share this dataset

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.