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ACSS2 modulates endothelial glycolysis in angiogenesis

GSE301613 Homo sapiens (human) RNA-seq (gene expression) 9 samples Submitted 2026/06/01 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 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
Homo sapiens (human)
Samples
9 samples: 3 × Primary HUVECs, Scramble siRNA, 6 days, 1% O2 30h vs 3 × Primary HUVECs, ACSS2 siRNA, 6 days, 1% O2 30h vs 3 × Primary HUVECs, ACSS2 + PDK4 siRNA, 6 days, 1% O2 30hGroups 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)
Endothelial cells (ECs) sustain high glycolytic flux and display remarkable metabolic plasticity. Although the molecular pathways regulating endothelial glycolysis are well characterized, the metabolic mechanisms underlying hypoxia-induced glycolytic activation during angiogenesis remain poorly understood. Here, we show that acetyl-CoA synthetase 2 (ACSS2) serves as a critical metabolic modulator, coupling acetate utilization with glycolytic flux to control EC function and angiogenesis.
Read the full summary ↓
The high level of ACSS2-mediated acetate-to-acetyl-CoA conversion in angiogenic front ECs sustains acetyl-CoA levels, which are essential for EC proliferation and retinal vascularization. Conversely, endothelial-specific Acss2 deletion disrupts pathological angiogenesis and normalizes tumor vasculature. Mechanistically, ACSS2 maintains hypoxia-inducible factor 1α transcriptional activity and stabilizes glucose transporter 1, thereby preserving glycolysis. Pyruvate dehydrogenase kinase 4 knockdown rescues metabolic and functional defects in ACSS2-deficient ECs, revealing acetyl-CoA homeostasis as a lynchpin of hypoxic endothelial metabolism. Collectively, our work establishes ACSS2 as a pivotal regulator of vascular development and proposes targeting acetate metabolism as a strategy to modulate pathological angiogenesis.
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 GSE301613_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 PRJNA1285789 and SRA study SRP598037. Searching any of these in the dataset finder brings you back here.

Study design
3 × Primary HUVECs, Scramble siRNA, 6 days, 1% O2 30h vs 3 × Primary HUVECs, ACSS2 siRNA, 6 days, 1% O2 30h vs 3 × Primary HUVECs, ACSS2 + PDK4 siRNA, 6 days, 1% O2 30h

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.