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TJ0113 alleviates ferroptosis by improving mitochondria of renal tubules in the transition from AKI to CKD

GSE286531 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/07/31 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × C vs 3 × S vs 3 × XGroups 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)
Acute kidney injury (AKI) is a prevalent clinical complication with a high risk of progression to chronic kidney disease (CKD), yet effective drugs to prevent or treat the transition from AKI to CKD are still lacking. The kidney is an organ rich in mitochondria and mitochondrial dysfunction plays a pivotal role in the progression from AKI to CKD.
Read the full summary ↓
In this study, we established a mouse model of bilateral renal artery ischemia-reperfusion injury to investigate whether TJ0113, a mitophagy inducer currently in Phase 2 of clinical trials (NCT06596005), can be used to mitigate the transition from AKI to CKD. We found that TJ0113 improved the high mortality rate and renal dysfunction in AKI mice, alleviated renal injury, inflammation, and interstitial fibrosis during the transition from AKI to CKD, and improved mitochondrial quality in renal tubules. RNA-seq results showed that TJ0113 reduced the expression of activating transcription factor 3 (ATF3), which is upstream of the classic ferroptosis pathway. In summary, our data show that TJ0113 maintains mitochondrial quality in renal tubules through mitophagy, thereby improving the progression from AKI to CKD, and represents a potential drug for preventing and treating the transition from AKI to 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 GSE286531_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 PRJNA1209871 and SRA study SRP556982. Searching any of these in the dataset finder brings you back here.

Study design
3 × C vs 3 × S vs 3 × X

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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.