New research identifies a direct signalling axis from beige fat to blood vessels that can raise blood pressure independently of obesity. The team began from clinical links between brown fat and lower hypertension risk and then removed Prdm16 only in adipocytes to erase beige fat identity while keeping mice metabolically healthy. This targeted approach isolated the effect of beige fat loss from obesity and inflammation.
When beige identity was lost, perivascular fat lost its thermogenic features, adopted a white-fat profile and began expressing angiotensinogen, a precursor of a hormone that increases vascular tone. The engineered mice developed higher blood pressure and mean arterial pressure. Histology and sequencing showed fibrous extracellular material accumulating around vessels and a vascular cell program promoting fibrosis. Isolated arteries were unusually sensitive to angiotensin II.
Analysis of secreted factors identified the enzyme QSOX1 as overproduced by altered adipocytes; beige fat normally keeps QSOX1 suppressed. In mice lacking both Prdm16 and Qsox1 the vascular remodeling and hypertension did not occur. Large clinical cohorts also showed higher blood pressure in people with PRDM16 mutations. The findings, published in Science and reported by Rockefeller University, point to QSOX1 as a potential target for future therapies and motivate studies on how QSOX1 reshapes vessel scaffolding and alters angiotensin receptor function.
Difficult words
- axis — a pathway connecting parts that sends biological signals
- perivascular — located around or surrounding a blood vessel
- thermogenic — producing heat in a tissue or organism
- angiotensinogen — a protein precursor that helps make a blood hormone
- fibrosis — formation of excess connective tissue in an organ
- extracellular — located outside the cells in body tissues
- remodel — to change the structure or form of somethingremodeling
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Discussion questions
- How could targeting QSOX1 change future treatments for high blood pressure? Give possible benefits and risks.
- Why did the researchers remove Prdm16 only in adipocytes instead of studying obese animals? Explain the experimental advantage.
- What further experiments would you propose to learn how altered adipocytes reshape vessel scaffolding or change receptor function?
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