Overview
- Researchers deleted the Prdm16 gene specifically in adipocytes to strip beige fat identity while avoiding confounders such as obesity or inflammation.
- Mice lacking beige fat developed higher blood pressure and mean arterial pressure along with perivascular fibrosis and heightened sensitivity to angiotensin II.
- Secretome analyses identified the enzyme QSOX1 as the key mediator released by beige-fat–deficient adipocytes that drives vascular remodeling.
- Engineering double-knockout mice lacking both Prdm16 and Qsox1 prevented vascular dysfunction and normalized blood pressure, implicating QSOX1 as causal.
- Meta-analyses of human cohorts linked PRDM16 variants to higher blood pressure, pointing to adipose–vascular signaling as a promising, though still unproven, therapeutic avenue.