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Human iPSC-cardiomyocyte models of insulin resistance demonstrate metabolic and contractile dysfunction that recapitulates diabetic cardiomyopathy

GSE288708 Homo sapiens (human) RNA-seq (gene expression) 20 samples Submitted 2025/06/16 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 20 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
20 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.
Paper
FoxO1-zDHHC4-CD36 S-Acylation Axis Drives Metabolic Dysfunction in DiabetesCirculation research · 2025
Summary (written by the submitters)
In type II diabetes (T2DM), the heart is exposed to hyperglycaemia, hyperlipidaemia, and hyperinsulinaemia, leading to insulin resistance and metabolic dysfunction, culminating in diabetic cardiomyopathy (DbCM). Human-centric models of DbCM are needed to provide mechanistic insights and therapeutic targets in a translationally relevant setting.
Read the full summary ↓
We hypothesised that culturing human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) in an “insulin resistance” (IR) media, and assessing this using a systems biology approach, would offer a comprehensive evaluation of dysregulated pathways, establishing their suitability as a model of DbCM. Culturing 2D hiPSC-CMs in IR media induced insulin resistance and activated pathways implicated in DbCM, including metabolic remodelling, mitochondrial dysfunction, and endoplasmic reticulum stress. Adaptation to hypoxia, a key component of post-ischaemic remodelling, was blunted in the 2D IR hiPSC-CMs, highlighting impaired cellular responses to low oxygen conditions. Proteomic and transcriptomic analyses revealed significant enrichment of DbCM-related pathways, particularly those involved in metabolic dysregulation. In conclusion, 2D hiPSC-CMs cultured in IR media recapitulate key features of DbCM, including impaired adaptation to hypoxia, providing a valuable model for studying diabetic cardiomyopathy.
Published in
FoxO1-zDHHC4-CD36 S-Acylation Axis Drives Metabolic Dysfunction in Diabetes
Dennis KMJH, Gopal K, Montes Aparicio CN et al. · Circulation research 2025 · PMID 40357580 · doi:10.1161/CIRCRESAHA.124.325918
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 GSE288708_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 PRJNA1219113 and SRA study SRP561490. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 20 more — browse all 20 samples with per-sample file links →

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