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Sodium myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis in pressure overloaded mouse hearts

GSE245135 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/01/08 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 5 × WT two weeks post TAC vs 5 × Smit1-/- two weeks post TACGroups 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)
Sodium myo-inositol cotransporter-1 (SMIT1) belongs to the sodium-glucose cotransporter family and accounts for intracellular accumulation of myo-inositol. SMIT1 is expressed in the heart, where its function remains unknown. Here, we demonstrate the contribution of SMIT1 to pathological hypertrophic cardiac remodeling and the progression to heart failure, using a mouse model of pressure overload induced by transverse aortic constriction.
Read the full summary ↓
We found that aortic banding failed to induce systolic dysfunction, cardiac hypertrophy and fibrosis in mice lacking SMIT1 (Smit1-/-), in contrast to wild type controls. SMIT1 genetic deletion reduced cardiac O-GlcNAcylation, which normally increases following hemodynamic stress, and restored ions homeostasis preventing the resulting pro-hypertrophic transcriptional reprogramming. This work provides important insights into the role of SMIT1 at the onset of heart failure, opening new avenues of potential therapeutic strategy to prevent or treat pathological hypertrophy and heart failure.
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 GSE245135_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 PRJNA1026990 and SRA study SRP465821. Searching any of these in the dataset finder brings you back here.

Study design
5 × WT two weeks post TAC vs 5 × Smit1-/- two weeks post TAC

Supports a between-group comparison across 10 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 10 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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