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Transient Senescence Following Myocardial Infarction: Characterization and Functional Implications in Cardiac Remodeling [snMultiome]

GSE296300 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 8 samples Submitted 2026/09/01 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 8 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Samples
8 samples
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)
Recent studies suggest that transient premature senescence is essential for tissue remodeling. Myocardial infarction (MI) induces extensive myocardial remodeling through fibroblast-driven extracellular matrix (ECM) production. However, the characteristics and functions of the senescent cells (Sen.) following MI-induced cardiac remodeling remains elusive.
Read the full summary ↓
In the present study, we observed a gradual increment number of Sen. within the ischemic region over time following MI, peaking at day 7 post-MI, with a subsequent decline in both wild-type mice and p16Ink4a-CreERT2-mT/mG reporter mice within 4 weeks. Using lineage tracing in the p16 reporter mice, we found most of the transient Sen. transitioned to non-senescent state. Then we analyzed our single-nucleus (sn)-multiome and fluorescence-based (SPiDER-β-gal/p16-EGFP) spatial transcriptomics data from the infarcted heart on day 7 post-MI to identify the cellular composition of transient Sen. We also conducted the deconvolution of the Sen. in the integrated dataset using different computational techniques. Additionally, we generated a reference (query dataset) based on SPiDER-βGal/p16-EGFP positivity and mapped it back to the snMultiome dataset. Through all approaches, we found fibroblasts and the subpopulation late myofibroblasts (MF) constituted a major proportion of Sen. In the snMultiome dataset, we explored the features of senescent late MF through differentially expressed genes/peaks and transcriptional binding motif analysis, and found the senescent late MF exhibited enhanced contractile properties and reduced ECM production capability compared with non-senescent late MF. These findings were supported by in vitro experiments showing that ischemia-induced senescent MF exhibited reduced soluble collagen production compared to TGF-β1-induced non-senescent MF. Additionally, in vivo studies revealed worsened cardiac function post-MI following senolytics administration compared to the vehicle group.
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 GSE296300_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1258881 and SRA study SRP583082. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 8 more — browse all 8 samples with per-sample file links →

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