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ALDH2 inhibition reprograms tubular epithelial cell metabolism and promotes renal injury susceptibility

GSE306861 Mus musculus (mouse) RNA-seq (gene expression) 8 samples Submitted 2026/08/05 Platform GPL24247
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: 4 × WT primary TECs vs 4 × KO primary TECsGroups 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)
Tubular epithelial cells (TECs), viewed as the initiating factor in renal fibrosis, undergo a transition from re-absorptive to pro-fibrotic phenotype during chronic kidney disease (CKD) progression. Serving as a critical energy source, Free fatty acid (FFA) metabolism disruption results in injured TECs. Nevertheless, mechanisms underlying pathological FFA metabolism in injured TECs remain unclear.
Read the full summary ↓
We observed an inverse correlation between ALDH2 expression in TECs and lipid deposition in the renal tissues from CKD patients. To determine whether ALDH2 protects against fibrosis via regulating FFA metabolism, we generated TEC–specific ALDH2 knockout (Aldh2TEC-KO) mice, and observed exacerbated fibrosis and lipid deposition in the renal tissues of Aldh2TEC-KO mice in two different CKD models. Mechanically, we verified that ALDH2 facilitated the formation of PPARα/RXRα heterodimer via nuclear translocation, while ALDH2 deficiency hindered that process, suppressed PPARα/RXRα complex activation, and disrupted fatty acid oxidation. Notably, Fenofibrate, the PPARα-specific agonist, failed to alleviate fibrosis or lipid deposition in the renal tissues from Aldh2TEC-KO mice, indicating that ALDH2 deficiency attenuated Fenofibrate's efficacy. Furthermore, the ALDH2 E487K mutation similarly impaired FFA metabolism and promoted fibrotic phenotype. Together, this work uncovers ALDH2 as a novel FAO regulator and an influencing factor of Fenofibrate therapeutic efficacy in CKD.
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 GSE306861_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 PRJNA1312710 and SRA study SRP614715. Searching any of these in the dataset finder brings you back here.

Study design
4 × WT primary TECs vs 4 × KO primary TECs

Supports a between-group comparison across 8 samples.

How we read this: 2 replicated groups read from 8 sample titles; they account for 8 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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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.