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Redox Regulation of Lung Endothelial PERK, Unfolded Protein Response (UPR) and Proliferation via NOX1: Targeted Inhibition as a Potential Therapy for PAH

GSE291410 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/03/10 Platform GPL34281
At a glance

RNA-seq (gene expression) · human · 12 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
Homo sapiens (human)
Samples
12 samples: 3 × HPAEC_NORMOXIA_siCT vs 3 × HPAEC_NORMOXIA_siNOX1 vs 3 × HPAEC_HYPOXIA_siCT vs 3 × HPAEC_HYPOXIA_siNOX1Groups 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
Redox regulation of lung endothelial PERK, unfolded protein response (UPR) and proliferation via NOX1: Targeted inhibition as a potential therapy for PAHRedox biology · 2025
Summary (written by the submitters)
Aims: Reactive oxygen species (ROS) play an important role in the pathogenesis of pulmonary arterial hypertension (PAH) and NADPH oxidases (NOXs) as sources of ROS are implicated in the development of the disease. We previously showed that NOX isozyme 1 (NOX1)-derived ROS contributes to pulmonary vascular endothelial cell (EC) proliferation in response to PAH triggers in vitro.
Read the full summary ↓
However, whether and how NOX1 is involved in PAH in vivo have not been explored nor has NOX1 been examined as a viable and effective therapeutic disease target. Methods and Results: Herein, infusion of mice exposed to Sugen/hypoxia (10% O2) with a specific NOX1 inhibitor, NOXA1ds, delivered via osmotic minipumps (i.p.), significantly suppressed pathological changes in hemodynamic parameters characteristic of PAH. Furthermore, lungs of human patients with idiopathic PAH (iPAH) and exploratory RNA-seq analysis of hypoxic human pulmonary ECs, in which NOX1 was suppressed, were probed. The findings showed a clear indication of NOX1 in the promotion of both protein disulfide isomerase (PDI) and the unfolded protein response (UPR; in particular, the PERK arm of the pathway including eIF2α and ATF4) leading to proliferation. In aggregate, these results are consistent with a causal role for NOX1 in the development of mouse and human PAH and reveal a novel and mechanistic pathway by which NOX1 activates the UPR response during EC proliferation. Conclusion: NOX1 promotes phenotypic changes in ECs that are pivotal to proliferation and PAH through activation of the UPR. Taken together, our results are consistent with selective inhibition of NOX1 as a novel modality for attenuating PAH
Published in
Redox regulation of lung endothelial PERK, unfolded protein response (UPR) and proliferation via NOX1: Targeted inhibition as a potential therapy for PAH
Goossen CJ, Kufner A, Dustin CM et al. · Redox biology 2025 · PMID 40154102 · doi:10.1016/j.redox.2025.103554
This dataset
Open GSE291410 in finder → Find more human 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 GSE291410_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 PRJNA1233320 and SRA study SRP568739. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40154102) ↗
Study design
3 × HPAEC_NORMOXIA_siCT vs 3 × HPAEC_NORMOXIA_siNOX1 vs 3 × HPAEC_HYPOXIA_siCT vs 3 × HPAEC_HYPOXIA_siNOX1

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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