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Pharmacological inhibition of GLUT1 alleviates fulminant hepatitis by restraining macrophage-induced inflammatory cascades and restoring metabolic homeostasis

GSE325494 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/03/25 Platform GPL13112
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × Ctrl vs 3 × D-gal-LPS vs 3 × WZB-D-gal-LPSGroups 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)
Fulminant hepatitis (FH) is a life-threatening clinical syndrome characterized by massive hepatocyte necrosis and rapid liver failure, with limited therapeutic options beyond transplantation. Although hepatic macrophages are known to drive FH immunopathology, the metabolic mechanisms governing their hyperactivation remain poorly understood.
Read the full summary ↓
In this study, we investigated the role of glucose transporter 1 (GLUT1)-mediated metabolic reprogramming in the progression of D-gal/LPS-induced FH. GLUT1 is significantly upregulated in hepatic macrophage during acute injury, facilitating a shift toward aerobic glycolysis. This glycolytic surge, regulated via the PI3K/AKT signaling pathway, serves as a fundamental driver for pro-inflammatory M1 macrophage polarization and the subsequent cytokine storm. Notably, pharmacological inhibition of GLUT1 with WZB117 effectively suppressed glycolytic flux, attenuated M1-type activation, and restored lipid metabolic homeostasis, thereby significantly reducing hepatocellular apoptosis and systemic inflammation. Transcriptomic and metabolomic profiling confirmed that GLUT1 inhibition rebalances the immune microenvironment by intercepting the macrophage-mediated inflammatory cascade at its inception. Collectively, these findings identify GLUT1 as a pivotal molecular switch in macrophage-intrinsic metabolic reprogramming and suggest that targeting GLUT1-mediated glycolysis represents a promising therapeutic strategy for the clinical management of fulminant hepatic failure.
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 GSE325494_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 PRJNA1440342 and SRA study SRP685378. Searching any of these in the dataset finder brings you back here.

Study design
3 × Ctrl vs 3 × D-gal-LPS vs 3 × WZB-D-gal-LPS

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.