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Targeting NPM1 Epigenetically Promotes Post-infarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism [RNA-Seq]

GSE230944 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2026/01/26 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 16 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
16 samples: 6 conditions, mostly in triplicateGroups 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.
Paper
Targeting NPM1 Epigenetically Promotes Postinfarction Cardiac Repair by Reprogramming Reparative Macrophage MetabolismCirculation · 2024
Summary (written by the submitters)
Background: Post-infarction heart failure is attributed to ischemia-induced myocardial inflammation and unfavorable remodeling, with reparative macrophages playing a crucial role in limiting excessive fibrosis and promoting cardiac repair via cytokine secretion and cross-cell interactions. Hence, a timely and adequate transition of macrophage phenotypes is essential for proper wound healing post-MI, but the precise mechanisms underlying this process remain incompletely elucidated.
Read the full summary ↓
Methods: To elucidate the function of NPM1 in post-infarct cardiac repair, we generated macrophage-specific NPM1 knockout mouse models. Additionally, Cut&Tag assays were conducted on cardiac macrophages for the first time to explore the epigenetic mechanisms underlying NPM1-mediated regulation of macrophage metabolic reprogramming. Results: Macrophage-specific deletion of NPM1 in MI mouse models resulted in reduced tissue fibrosis and enhanced cardiac repair by promoting the phenotypic transition of macrophages towards a reparative state. NPM1 deletion also led to a shift in macrophage metabolism from glycolysis to mitochondrial OXPHOS via inactivation of the mTOR cascades. Mechanistically, we demonstrated that IL-4 induced NPM1 oligomerization, which recruited histone demethylase KDM5b to the promoter region of Tsc1, ultimately leading to macrophage metabolic rewiring. Antisense oligonucleotides and inhibitory compounds targeting NPM1 exhibited notable protective effects on cardiac repair post-MI. Conclusions: Our study demonstrates that NPM1 may serve as a promising prognostic biomarker and a valuable therapeutic target for ischemia-induced heart failure, shedding new light on the understanding of post-infarct cardiac repair and may pave the way for the development of innovative therapeutic strategies.
Published in
Targeting NPM1 Epigenetically Promotes Postinfarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism
Zhang S, Zhang Y, Duan X et al. · Circulation 2024 · PMID 38390737 · doi:10.1161/CIRCULATIONAHA.123.065506
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 GSE230944_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 PRJNA962932 and SRA study SRP435099. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
ko cardiac macrophage, mi-d5, biol ×3 wt cardiac macrophage, mi-d5, biol ×3 ko cardiac macrophage, mi-d3, biol ×3 wt cardiac macrophage, mi-d3, biol ×3 ko cardiac macrophage, mi-d ×2 wt cardiac macrophage, mi-d ×2

Supports a between-group comparison across 16 samples.

How we read this: 6 replicated groups read from 16 sample titles; they account for 16 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.