GEO series

Effect of depletion of Endothelial Cell STING in response to pressure overload induced heart failure

GSE296709 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2025/06/12 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 15 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: 15 samples: 15 samples, each with a distinct title — no replicated groupsGroups 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: Endothelial Cell Stimulator of Interferon Genes Regulates IL-6 Production and Is Required for Pathologic Cardiac Hypertrophy and Contractile Dysfunction in Experimental Heart FailureThe American journal of pathology · 2025

Summary (written by the submitters)

Capillary rarefaction and cardiomyocyte (CM) hypertrophy are hallmarks of the complex syndrome of heart failure (HF), a leading cause of hospitalization and death. Molecular signals within and between cellular components of the heart have emerged as central hubs that modulate cardiac pathophysiology. Here, we discovered that the Stimulator of Interferon Genes (STING) is highly expressed in human and mouse cardiac endothelial cells (EC) and is activated in the onset of HF.

Read the full summary ↓

Using global and inducible EC-specific STING-/- mice, we report that EC STING is required for contractile dysfunction in an experimental model of HF induced by transverse aortic constriction (TAC), through the regulation of CM hypertrophy and capillary rarefaction. We report that ECs sorted from TAC EC-STING-/- mice are enriched in gene sets related to integrin and cell adhesion pathways to extracellular matrix (ECM) compared to controls and have decreased expression of the pro-hypertrophic gene IL-6. CellChat analysis of human cardiac cells from patients with non-ischemic cardiomyopathy revealed EC-CM communication, and mechanistically, we found that STING activation induces IL-6 secretion, and that EC derived IL-6 is necessary to induce pro-hypertrophic gene expression in CMs in a STING dependent manner. Our study demonstrates a novel role for STING in ECs contributing to hypertrophy and contractile dysfunction in experimental HF.

Published in

Endothelial Cell Stimulator of Interferon Genes Regulates IL-6 Production and Is Required for Pathologic Cardiac Hypertrophy and Contractile Dysfunction in Experimental Heart Failure

Sanders E, Kaur K, Wagner N et al. · The American journal of pathology 2025 · PMID 40639717 · doi:10.1016/j.ajpath.2025.06.004

This dataset

Open GSE296709 in finder → Find more mouse RNA-seq datasets →

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.

Series matrix ↓

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 GSE296709_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA1260809 and SRA study SRP584109. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40639717) ↗

Study design

15 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 15 sample titles: 15 distinct titles with little repetition. 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

GSM8975157 EC, 131 WT_Sham, 4 weeks
GSM8975158 EC, 132 WT_Sham, 4 weeks
GSM8975159 EC, 133 WT_Sham, 4 weeks
GSM8975160 EC, 134 WT_TAC, 4 weeks
GSM8975161 EC, 135 WT_TAC, 4 weeks
GSM8975162 EC, 136 WT_TAC, 4 weeks
GSM8975163 EC, 137 WT_TAC, 4 weeks
GSM8975164 EC, 138 WT_TAC, 4 weeks
GSM8975165 EC, 348 EC KO_Sham, 4 weeks
GSM8975166 EC, 349 EC KO_Sham, 4 weeks
GSM8975167 EC, 350 EC KO_Sham, 4 weeks
GSM8975168 EC, 351 EC KO_TAC, 4 weeks
GSM8975169 EC, 352 EC KO_TAC, 4 weeks
GSM8975170 EC, 353 EC KO_TAC, 4 weeks
GSM8975171 EC, 354 EC KO_TAC, 4 weeks

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GSE316502 Transcriptomic Profiling of the Sex-linked Biological Pathways of Severe Pulmonary Arterial Hypertension associated with Endothelial Cell Caveolin-1 Depletion and Chronic Hypoxia 35 samples shares endothelial, depletion
GSE328371 KMT2D depletion promote KRAS-induced pancreatic carcinogenesis independent of TP53 24 samples shares depletion, induced

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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.