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Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction

GSE306012 Mus musculus (mouse) RNA-seq (gene expression) 28 samples Submitted 2026/07/22 Platform GPL30172
At a glance

RNA-seq (gene expression) · mouse · 28 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
28 samples: 8 conditions, mostly with about 4 replicates eachGroups 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
Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarctionCardiovascular research · 2026
Summary (written by the submitters)
Myocardial infarction (MI) triggers a complex remodelling process that leads to heat failure if uncontrolled. A Disintegrin and metalloproteinase-17 (ADAM17), a transmembrane sheddase, is upregulated in patients with ischemic cardiomyopathy, colocalized to myofibroblasts (myoFB) in the infarct tissues. Fibroblasts are key players in post-MI scar formation and exist in different states with diverse functions.
Read the full summary ↓
Using mice with inducible Adam17 deletion in homeostatic FBs (Adam17 FB-KD ), or activated FBs (Adam17 myoFB-KD ), we found that ADAM17 loss in homeostatic FBs impaired infarct formation post-MI and increased mortality due to left ventricular (LV) rupture. Conversely, ADAM17 loss in myoFBs limited infarct expansion, LV dilation and dysfunction up to 4 weeks post-MI. Ex vivo and in vitro experiments revealed that the beneficial effects in Adam17 myoFB-KD mice are due to reduced stiffness of the infarct tissue through suppressing activation of EGFR-YAP-pathway, which promoted vascularization and thereby limited infarct expansion. Pharmacological inhibition of ADAM17 prior to MI was ineffective, but short-term ADAM17 inhibition after MI by targeting myoFBs significantly alleviated the adverse LV remodeling and dysfunction with beneficial effects up to 4wks post-MI. Our study identifies a short-term therapeutic window for ADAM17 inhibition to prevent long-term adverse remodeling, dysfunction and heart failure post-MI.
Published in
Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction
Li Y, Al Rimon R, Wang F et al. · Cardiovascular research 2026 · PMID 41524432 · doi:10.1093/cvr/cvaf256
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 GSE306012_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 PRJNA1308956 and SRA study SRP610700. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly with about 4 replicates each
Mouse Cardiac Fibroblast, Hypoxia, Adam17 siR… ×4 Mouse Cardiac Fibroblast, Hypoxia, Control, ×4 Mouse Cardiac Myofibroblast, Hypoxia, Adam17 … ×4 Mouse Cardiac Myofibroblast, Hypoxia, Control, ×4 Mouse Cardiac Fibroblast, Normoxia, Adam17 si… ×3 Mouse Cardiac Fibroblast, Normoxia, Control, ×3 Mouse Cardiac Myofibroblast, Normoxia, Adam17… ×3 Mouse Cardiac Myofibroblast, Normoxia, Contro… ×3

Supports a between-group comparison across 28 samples.

How we read this: 8 replicated groups read from 28 sample titles; they account for 28 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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