GEO series

HSD17B13 Deficiency Modulates Interferon Signaling to Ameliorate Metabolic Dysfunction-Associated Steatohepatitis Fibrosis

GSE242672 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/06/30 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: 6 × CDAA-WT vs 6 × CDAA-KOGroups 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)

The discovery that loss-of-function variants in HSD17B13 are associated with protection from Metabolic dysfunction-associated steatohepatitis (MASH, previously known as NASH) and fibrosis led to the use of HSD17B13-targeting agents in clinical trials but the underlying mechanism remains unknown. We were able to phenocopy the human findings in Hsd17b13-knockout (KO) mice fed choline-deficient amino acid-defined high fat diet (CDAA-HFD).

Read the full summary ↓

Metabolomic and lipidomic analysis identified a beneficial shift in Hsd17b13-KO from lipotoxic cholesterol and ceramides to neutral lipids and sphingomyelins. Hepatic interferon signaling was upregulated in Hsd17b13-KO in parallel with the decrease in fibrosis. We confirmed in vitro that medium from Hsd17b13-depleted hepatocytes decreases hepatic stellate cell (HSC) activation. Hsd17b13 depletion was sufficient to induce hepatocyte interferon signaling, and induction of this pathway was sufficient to inhibit medium-exposed HSCs. We show that DiHOMEs, lipokines derived from linoleic acid, are likely the mediator by which HSD17B13 affects interferon signaling. Finally, we find a similar upregulation of hepatic interferon signaling in human subjects who carry the HSD17B13 rs72613567 loss-of-function variant. Collectively, our data suggest that loss of HSD17B13 attenuates MASH fibrosis through augmentation of protective hepatocyte interferon signaling to mitigate HSC activation. These findings shed new light on potential strategies to treat MASH-associated fibrosis.

This dataset

Open GSE242672 in finder → Find more mouse 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 GSE242672_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 PRJNA1014005 and SRA study SRP459147. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

6 × CDAA-WT vs 6 × CDAA-KO

Supports a between-group comparison across 12 samples.

How we read this: 2 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

GSM7766631 CDAA-WT-01 CDAA-WT
GSM7766632 CDAA-WT-02 CDAA-WT
GSM7766633 CDAA-WT-03 CDAA-WT
GSM7766634 CDAA-WT-04 CDAA-WT
GSM7766635 CDAA-WT-05 CDAA-WT
GSM7766636 CDAA-WT-06 CDAA-WT
GSM7766637 CDAA-KO-01 CDAA-KO
GSM7766638 CDAA-KO-02 CDAA-KO
GSM7766639 CDAA-KO-03 CDAA-KO
GSM7766640 CDAA-KO-04 CDAA-KO
GSM7766641 CDAA-KO-05 CDAA-KO
GSM7766642 CDAA-KO-06 CDAA-KO

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GSE254687 PARK7/DJ-1 deficiency modulates microglial activation in response to LPS-induced inflammation 19 samples shares deficiency, modulates
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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.