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Effect of vasostatin-2 treatment on gene expression in mouse femoral arteries following wire injury

GSE295298 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2025/09/01 Platform GPL23479
Summary
Neointimal hyperplasia is a major pathological process underlying restenosis following vascular injury. Vasostatin-2, a bioactive peptide derived from chromogranin A, has been implicated in vascular protection, but its mechanism remains unclear. To investigate the molecular basis through which vasostatin-2 modulates vascular remodeling, we performed transcriptomic profiling using RNA sequencing in a mouse model of femoral artery wire injury. Mice underwent wire-induced endothelial denudation of the femoral artery and immediately received perivascular treatment with either vasostatin-2 or saline. At 3 days post-injury, the injured femoral arteries were harvested for RNA-seq analysis to examine the impact of vasostatin-2 treatment on gene expression changes associated with vascular injury and neointima formation. This dataset provides insight into the transcriptional programs regulated by vasostatin-2 during the early phase of vascular injury and may reveal therapeutic targets for preventing restenosis.
Published in
Vasostatin-2 attenuates injury-induced neointimal hyperplasia through the ACE2/MasR/PPARγ/NR1D1/Gas1 axis
Chen Q, Liu J, Madonna R et al. · Cardiovascular research 2025 · PMID 41231769 · doi:10.1093/cvr/cvaf192
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Also filed as BioProject PRJNA1254148 and SRA study SRP580473. Searching any of these in the dataset finder brings you back here.

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