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Cardiac adaptation to endurance exercise training requires suppression of GDF15 via PGC-1α

GSE302867 Mus musculus (mouse) RNA-seq (gene expression) 20 samples Submitted 2025/07/20 Platform GPL17021
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
20 samples: 5 × WT_Sed vs 5 × KO_Sed vs 5 × WT_Ex vs 5 × KO_ExGroups 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)
Endurance exercise promotes adaptive growth and improved function of cardiomyocytes, which is supported by increased mitochondrial activity. In skeletal muscle, these benefits are coordinated by the transcriptional protein peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). The importance of PGC-1α to exercise-induced adaptations in the heart has been unclear.
Read the full summary ↓
Here, we show that deleting PGC-1α specifically in cardiomyocytes prevents the expected benefits from exercise and instead confers heart failure after just six weeks of training. Supporting this, rare genetic variants in the human PPARGC1A gene, which encodes PGC-1α, are associated with risk of heart failure in the UK Biobank. We identify the stress-induced cytokine growth-differentiation factor 15 (GDF15) as a key factor increased in PGC-1α–deficient hearts that contributes to this dysfunction. Blocking cardiac Gdf15 expression improves cardiac performance and exercise capacity in these mice. Finally, in human heart tissue, lower cardiomyocyte PGC-1α expression is associated with higher GDF15 and with fewer cardiomyocytes. These findings implicate a crucial role for cardiomyocyte PGC-1α in enabling healthy heart adaptation to exercise in part through suppression of GDF15.
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 GSE302867_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 PRJNA1292724 and SRA study SRP601476. Searching any of these in the dataset finder brings you back here.

Study design
5 × WT_Sed vs 5 × KO_Sed vs 5 × WT_Ex vs 5 × KO_Ex

Supports a between-group comparison across 20 samples.

How we read this: 4 replicated groups read from 20 sample titles; they account for 20 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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