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Gut microbiota-glycine-UCP3 axis modulates the protection of canagliflozin against cardiac hypertrophy

GSE347125 Mus musculus (mouse) RNA-seq (gene expression) 8 samples Submitted 2026/09/21 Platform GPL28330
At a glance

RNA-seq (gene expression) · mouse · 8 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
8 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.
Summary (written by the submitters)
Canagliflozin (CANA), a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, exert cardioprotective effects and improve long-term clinical outcomes in heart failure patients without diabetes. However, given negligible myocardial SGLT2 expression, the mechanisms remain unclear. Here, we found that CANA altered the community structure of gut microbiota in mice subjected to pressure overload.
Read the full summary ↓
Moreover, mice receiving microbiota transplants from TAC and CANA-treated mice exhibited better cardiac function compared to those receiving microbiota transplants from TAC-treated donors. Metabolite profiling identified glycine as a key mediator that protected against cardiac hypertrophy in mice. Importantly, the reduced glycine levels in hypertrophic mice were prevented by CANA treatment. We further demonstrated that Clostridium sp. was responsible for the degradation of glycine. Mechanistically, we showed that glycine activated the AMP-activated protein kinase α (AMPKα)/ peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) pathway, thus upregulating uncoupling protein 3 (UCP3) to preserve mitochondrial integrity and promote oxidative phosphorylation. UCP3 deficiency largely abolished the protective effect of CANA or glycine treatment against heart failure in mice. Our findings establish the gut microbiota-derived glycine/UCP3 signaling axis as a novel mechanism through which CANA exerts its anti-hypertrophic effects.
This dataset
Open GSE347125 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 GSE347125_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 PRJNA1524355 and SRA study SRP734037. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Samples in this study

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+ 8 more — browse all 8 samples with per-sample file links →

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