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Increased CPT1a expression is a critical cardioprotective response to pathological stress that suppresses gene programs for remodeling and enables rescue by gene transfer

GSE268251 Mus musculus (mouse) RNA-seq (gene expression) 30 samples Submitted 2026/01/21 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
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.
Paper
CPT1a Expression Is a Critical Cardioprotective Response to Pathological Stress That Enables Rescue by Gene TransferCirculation research · 2026
Summary (written by the submitters)
Carnitine palmitoyl transferase 1 (CPT1) is a rate-limiting enzyme for long chain fatty acid oxidation (FAO) in cardiac mitochondria. In adult hearts, CPT1b predominates, while CPT1a is co-expressed at lower levels. Pathological stress on the heart is known to induce CPT1a expression, but it’s role in pathological remodeling is unknown.
Read the full summary ↓
CPT1 isoform expression was assayed in myocardium of human heart failure (HF) patients with nonischemic cardiomyopathy (NICM). To explore the role of CPT1a upregulation in response to pathological stress, mice were subjected to cardiac pressure overload via transverse aortic constriction (TAC) or sham surgery (sham) with cardiac-specific CPT1a knockdown or cardiac-specific, AAV9 mediated overexpression of CPT1a (AAV9.cTNTN.Cpt1a). MiR370, known to suppress hepatic CPT1a, was also overexpressed to determine if miR370 regulates cardiac CPT1a expression. CPT1a protein was elevated and miR370 reduced in myocardium of male and female NICM patients (204% vs. non-failing unused donor hearts), as well as in failing mouse hearts. AAV mediated miR370 overexpression in mouse hearts suppressed CPT1a expression and attenuated the response of CPT1a to TAC. Preventing CPT1a upregulation in response to TAC in cardiac specific CPT1a knockout mice (csCPT1a ko) exacerbated adverse remodeling during TAC, causing severe dysfunction and increased mortality. In contrast, CPT1a overexpression (2.8 fold), attenuated impaired ejection fraction (EF, by 54%), fractional shortening (FS, 65%) and +/-dp/dt, and reduced ANP expression and heart mass/tibia length vs. PBS-infused TAC hearts (p<0.05). Delivery of AAV9.cTnT.Cpt1a 4 wks after TAC surgery during cardiac dysfunction, led to significant rescue of EF and FS vs. animals receiving empty virus and mitigated the exacerbated dysfunction of csCPT1a ko hearts at 4 wks TAC. RNA-seq and reverse transcription-quantitative PCR revealed a novel function of CPT1a in suppressing hypertrophic, profibrotic and cell death gene programs in both sham and TAC hearts, irrespective of changes in FAO. The effects of CPT1a in the heart extend beyond FAO and include a non-canonical regulation of cardiac gene programs. In addition to an animal model of HF, CPT1a upregulation occurs in failing human hearts, and is a critical and cardioprotective adaptation to pathological stress that attenuates adverse cardiac remodeling.
Published in
CPT1a Expression Is a Critical Cardioprotective Response to Pathological Stress That Enables Rescue by Gene Transfer
Carley AN, Maurya SK, Maurya CK et al. · Circulation research 2026 · PMID 41342119 · doi:10.1161/CIRCRESAHA.125.327403
This dataset
Open GSE268251 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 GSE268251_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 PRJNA1115794 and SRA study SRP509538. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41342119) ↗
Study design
8 conditions, mostly with about 4 replicates each
Heart, 8wks, FF Sham ×4 Heart, 8wks, FF TAC ×4 Heart, 8wks, KO Sham ×4 Heart, 8wks, TAC Sham ×4 Heart, 8wks, AAV9.Cpt1a Sham ×4 Heart, 8wks, AAV9.Cpt1a TAC ×4 Heart, 8wks, PBS Sham ×3 Heart, 8wks, PBS TAC ×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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