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Thymosin β4 alleviates sepsis-associated acute kidney injury by suppressing MAPK signaling pathway

GSE328666 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/07/16 Platform GPL24247
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 × LPS vs 3 × LTGroups 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)
Sepsis-associated acute kidney injury (SA-AKI) is a common complication in septic patients and is associated with high mortality and progression to chronic kidney disease (CKD). Previous studies have demonstrated that thymosin β4 (Tβ4) attenuates lipopolysaccharide (LPS)-induced liver injury and ischemic AKI via inhibiting inflammatory response.
Read the full summary ↓
Here, we aimed to investigate the effects of Tβ4 on SA-AKI and elucidate its underlying mechanisms. In vivo and in vitro models of SA-AKI were established using LPS. Tβ4 was administered 30 min after LPS exposure. Transcriptome sequencing was performed to explore the underlying molecular mechanisms, which were further validated by western blotting in vitro. In SA-AKI mice, serum Tβ4 levels were markedly decreased. Administering Tβ4 significantly ameliorated the renal dysfunction and morphological injury in LPS-treated mice. Consistently, Tβ4 reduced renal inflammation and apoptosis in SA-AKI mice. Transcriptome-sequencing analysis indicated that MAPK signaling pathway was involved in both SA-AKI pathogenesis and the protective effect of Tβ4. Western blotting of the renal tissues confirmed that LPS markedly increased the phosphorylation of JNK1/2, p38 MAPK and ERK1/2, whereas Tβ4 significantly suppressed their activation. Furthermore, pharmacological activation of MAPK pathway with anisomycin abrogated the inhibitory effects of Tβ4 on MAPK signaling in in vitro SA-AKI models. In conclusion, Tβ4 alleviates renal inflammation and apoptosis in SA-AKI by suppressing MAPK signaling pathway. Tβ4 may represent a potential therapeutic strategy for early intervention in SA-AKI.
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 GSE328666_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 PRJNA1456092 and SRA study SRP693611. Searching any of these in the dataset finder brings you back here.

Study design
3 × CTRL vs 3 × LPS vs 3 × LT

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.