GEO series

Formylpeptide Receptor Activation Attenuates Renovascular Remodeling in Neurogenic Hypertension (Kidney)

GSE333587 Mus musculus Expression profiling by high throughput sequencing 19 samples Submitted 2026/07/07 Platform GPL24247

Summary

Inflammation and sympathetic overactivity contribute to end-organ injury associated with hypertension. We previously demonstrated that targeting formylpeptide receptors (FPRs), which regulate and resolve inflammation, prevents cardiovascular damage in preclinical hypertension. Here, we investigated whether the FPR agonist Cmpd17b can reverse renovascular remodeling in established essential hypertension. Cmpd17b selectively reduced blood pressure in BPH/2J mice and improved aortic distensibility without altering cardiac function. Cmpd17b reduced collagen deposition across organs, most prominently in the kidney. RNA sequencing revealed kidney-specific upregulation of Serpina1e and Igfbp2, normalized by Cmpd17b. These findings identify FPR agonism as a promising therapeutic strategy for lowering blood pressure and reversing renovascular fibrosis.

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Direct links to NCBI, no account and no request form: the whole study as GSE333587_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 19 samples. Raw sequencing reads are also available from ENA.

Whole study · RAW.tar ↓ Series matrix ↓ All supplementary files ↗ Raw reads on ENA ↗

Also filed as BioProject PRJNA1471624 and SRA study SRP704444. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

19 conditions, each sampled once — no replicated groups

Supports a case/control comparison: 10 samples read as cases, 9 as controls.

Read from 19 sample titles: 19 distinct titles with little repetition. Check it against the sample list below before relying on it.

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