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Irx3 ameliorates postmyocardial infarction cardiac dysfunction by regulating both inflammatory and fibrotic pathways

GSE319045 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/02/16 Platform GPL34290
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: 4 × AAV9_Ctrl_Sham vs 4 × AAV9_Ctrl_MI vs 4 × AAV9_Irx3_MIGroups 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 Iroquois homeobox transcription factor Irx3 is associated with metabolic and hematologic disorders, but its role in cardiac repair after myocardial infarction (MI) remains unclear. This study found that Irx3 expression is significantly downregulated in the hearts of wild-type mice post-MI and in human AC16 cardiomyocytes under oxygen-glucose deprivation (OGD) conditions.
Read the full summary ↓
Overexpression of Irx3 improved cardiac function, reduced infarct size and myocardial fibrosis, attenuated inflammatory cell infiltration, prolonged survival in MI mice, and suppressed collagen synthesis and proinflammatory cytokine secretion in vitro. Mechanistically, Irx3 directly targets Srpx2 and Ppm1l: it downregulates Srpx2 to enhance AP-1 activity, increase SMAD7 expression, and inhibit TGF-β/SMAD signaling to limit fibrosis; it upregulates Ppm1l to interact with IKKβ, suppress NF-κB signaling, and reduce inflammatory cytokines (IL-1β, IL-6, TNF-α). RNA sequencing (RNA-seq) of mouse left ventricular tissues and Irx3-overexpressing AC16 cells identified differentially expressed genes enriched in extracellular matrix (ECM) remodeling and inflammation-related pathways, confirming Irx3’s coordinate regulation of profibrotic and proinflammatory pathways. These findings highlight Irx3 as a promising therapeutic target for post-MI cardiac repair and functional recovery.
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 GSE319045_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 PRJNA1422016 and SRA study SRP676119. Searching any of these in the dataset finder brings you back here.

Study design
4 × AAV9_Ctrl_Sham vs 4 × AAV9_Ctrl_MI vs 4 × AAV9_Irx3_MI

Supports a between-group comparison across 12 samples.

How we read this: 3 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
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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.