Overview
- In Science, researchers report that adipocyte-specific deletion of Prdm16 in mice erased beige fat identity, remodeled perivascular fat, and produced hypertension independent of obesity.
- Arteries from these mice showed heightened responsiveness to angiotensin II with increased vascular fibrosis and reduced flexibility.
- Loss of beige fat upregulated the secreted enzyme QSOX1, and concurrent Qsox1 deletion in Prdm16-deficient mice normalized vascular function and lowered blood pressure.
- A meta-analysis of genome-wide association data linked human PRDM16 variants to higher blood pressure, supporting translational relevance of the pathway.
- The work highlights QSOX1 inhibition or strategies that boost or stabilize beige fat as potential therapeutic avenues that require validation in human studies and clinical trials.