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Increased arrhythmic risk in obesity is transduced by adipose tissue-derived extracellular vesicles

GSE314750 Homo sapiens (human) RNA-seq (gene expression) 30 samples Submitted 2026/06/30 Platform GPL34284Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 30 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
Homo sapiens (human)
Samples
30 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.
Summary (written by the submitters)
While obesity is associated with atrial fibrillation and ventricular arrhythmias, whether direct communication from excess fat transduces this risk to the heart is unknown. Here, we demonstrate prolongation of the action potential duration (APD) is human atrial myocytes obtained from obese but not lean patients indicating obesity-associated electrical remodeling.
Read the full summary ↓
Consistent with this observation, visceral adipose tissue-derived extracellular vesicles (VAT EVs) from obese individuals similarly prolong action potential duration (APD) and impair calcium handling in human stem cell-derived cardiomyocytes, activate human cardiac fibroblasts and drive macrophages toward a pro-inflammatory phenotype, promoting a pro-arrhythmic substrate. We observed this communication in vivo, where adipose-derived EVs directly target cardiac cells in obese mice more than in lean mice, implicating a fat-heart communication axis in obesity. Human functional genomics anchored on genes differentially expressed in human cardiomyocytes, fibroblasts, and macrophages after human obese VAT-EV exposure identified targets causally linked to both QT interval (n=117,532) and atrial fibrillation (n= 181,446). Pharmacological blockade of a VAT-EV induced ion channel TRPC3 in cardiomyocytes restored the APD toward normal. These results collectively implicate an EV-mediated direct communication pathway between adipose tissue and the heart in arrhythmogenesis that activates both known and novel pathways, offering a new paradigm to identify mediators of cardiovascular disease in obesity.
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 GSE314750_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 PRJNA1392544 and SRA study SRP657379. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly with about 4 replicates each
iPSC-vCMs + VAT EVs # ×5 iPSC-CFs + iPSC-CF EVs # ×4 iPSC-CFs + VAT EVs # ×4 macrophages + macrophage EVs # ×4 iPSC-aCMs + VAT EVs # ×4 iPSC-vCMs + iPSC-vCM EVs # ×3 macrophages + VAT EVs # ×3 iPSC-aCMs + iPSC-aCM EVs # ×3

Supports a between-group comparison across 30 samples.

How we read this: 8 replicated groups read from 30 sample titles; they account for 30 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.