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Therapeutic targeting of lipidated amino acid deficiency ameliorates MASH via a PPARα/CCL2 axis

GSE304787 Mus musculus (mouse) RNA-seq (gene expression) 14 samples Submitted 2026/07/01 Platform GPL15103
At a glance

RNA-seq (gene expression) · mouse · 14 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
14 samples: 4 × Male CD vs 3 × Male MASH vs 3 × Male MASH OA vs 2 × Male MASH OALGroups 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)
Metabolic dysfunction-associated steatohepatitis (MASH), affects nearly one-third of the global population with limited pharmacotherapy approved, underscoring the urgent need for new therapeutic strategies. N-acyl amino acids (NAAs), comprising amino acids linked to long-chain fatty acid acyl groups, are gaining interest, yet their metabolic regulation in MASH remains elusive.
Read the full summary ↓
Metabolomic profiling in mice and humans with MASH revealed a marked depletion of NAAs, particularly C18:1-Leu, which inversely correlated with disease severity. The bidirectional PM20D1 expression was suppressed in the livers of human and mice with MASH, as well as in lipid-loaded primary mouse hepatocytes and hepatic cell lines. Stable isotope tracing studies in mice with and without MASH confirmed reduced biosynthesis of C18:1-Leu. Genetically, hepatocyte-specific overexpression of PM20D1 or pharmacological treatment with exogenous C18:1-Leu significantly attenuated or reversed established MASH. Mechanistically, C18:1-Leu bound and activated peroxisome proliferator-activated receptor alpha (PPARα), enhancing fatty acid β-oxidation and suppressing the NF-κB/CCL2 axis, thereby reducing hepatic macrophage infiltration, inflammation, and fibrosis. These therapeutic effects were abolished in hepatocyte-specific PPARα- and CCL2-deficient mice, identifying C18:1-Leu as a promising metabolic therapy for MASH.
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 GSE304787_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 PRJNA1302526 and SRA study SRP607109. Searching any of these in the dataset finder brings you back here.

Study design
4 × Male CD vs 3 × Male MASH vs 3 × Male MASH OA vs 2 × Male MASH OAL

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 14 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
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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.