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Atorvastatin regulates hepatic transcriptome PXR dependently but distinct from pregnenolone 16α-carbonitrile and does not induce PXR-mediated liver steatosis

GSE297644 Mus musculus (mouse) RNA-seq (gene expression) 24 samples Submitted 2026/05/19 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 24 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
24 samples: 24 samples, each with a distinct title — no replicated groupsGroups 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)
Several drugs induce liver steatosis through pregnane X receptor (PXR)-mediated mechanism. Atorvastatin is a PXR ligand but is still safe even in patients with metabolic dysfunction-associated steatotic liver disease. To reveal differences between atorvastatin and other PXR ligands, we characterized the effect of atorvastatin on PXR-mediated gene regulation and liver steatosis in mice.
Read the full summary ↓
Mice were treated orally with atorvastatin, a classical PXR ligand pregnenolone 16α-carbonitrile (PCN), or pravastatin, a statin not activating PXR. Atorvastatin treatment was also performed in PXR knockout mice. Analysis of liver transcriptomics after four-day treatment indicated that atorvastatin regulates genes almost exclusively through PXR. Atorvastatin and PCN regulated partially overlapping, but distinct set of genes and Cyp3a11 was not induced by atorvastatin. Pathway analysis indicated that the atorvastatin treatment predominantly induced genes involved in cholesterol synthesis, while PCN affected pathways involved in growth, proliferation, and steatosis. PCN increased nuclear SREBP1 protein level while atorvastatin increased both SREBP1 and SREBP2. In high-fat diet (HFD)-fed mice, 28-day oral treatment with PCN aggravated diet-induced liver steatosis while atorvastatin had no effect. 28-day atorvastatin treatment reduced the hepatic expression of PXR, and its effect on cholesterol synthesis genes disappeared. PCN did not influence PXR expression, and the Cyp3a11 expression remained induced still after 28 days. Among the lipogenic genes studied, Scd1 was the only one significantly induced by PCN after 28-day treatment in the HFD-fed mice. In summary, atorvastatin regulates mouse liver transcriptomics PXR dependently but differently from PCN and represses PXR in long-term treatment in the HFD-fed mice. Unlike PCN, atorvastatin does not promote liver steatosis.
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 GSE297644_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 PRJNA1265605 and SRA study SRP586755. Searching any of these in the dataset finder brings you back here.

Study design
24 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 24 sample titles: 24 distinct titles with little repetition. 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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