A major international study, published in the journal , has revealed an unexpected role for fat tissue in the regulation of blood pressure and vascular health. Researchers , and , from the Cardiovascular Health Across the Lifespan Program at The Research Institute of the ɬ Health Centre (The Institute), are co-authors.
The study shows that beige fat—a metabolically active form of fat related to brown fat—does more than regulate energy balance. It also actively communicates with blood vessels, influencing how they function and respond to physiological signals that control blood pressure. Importantly, this effect occurs independently of body weight, offering new insight into why hypertension, or high blood pressure, can develop even in people who are not obese.
“High blood pressure is often viewed through the lens of obesity and metabolic disease,” says Dr. Touyz, senior scientist and Executive Director and Chief Scientific Officer at The Institute. “This work shows that the biology of fat tissue itself—how fat cells function and signal to blood vessels—can have a profound impact on cardiovascular health.”
Uncovering a new fat–blood vessel communication pathway
While previous studies had linked the presence of beige or brown fat to lower cardiovascular risk, the mechanisms behind this association remained unclear. In this study, the researchers combined genetic models, advanced molecular analyses and vascular physiology experiments to demonstrate a direct causal relationship between beige fat dysfunction and elevated blood pressure. They also showed that this process depends on a protein called PRDM16.
When beige fat cells lost their specialized function in experimental models, blood vessels became stiffer and more reactive, undergoing fibrotic remodeling that led to sustained increases in blood pressure. The team traced these changes to the release of a specific enzyme, QSOX1, produced by fat cells when beige fat function is lost.
“By identifying QSOX1 as a fat-derived factor that directly alters vascular structure and responsiveness, we were able to connect molecular changes in fat cells to measurable changes in blood vessel behavior,” explains Augusto Montezano, scientist at The Institute who contributed to the experimental and mechanistic analyses. “When we selectively blocked QSOX1 in fat cells, vascular function improved and blood pressure normalized, which was a striking result.”
The study further strengthens its findings by integrating human genetic and clinical data, showing that variations in genes linked to beige fat function are associated with hypertension and cardiovascular remodeling in people.
Together, these results highlight beige fat as an active regulator of cardiovascular health rather than a passive bystander. By revealing how fat cell identity influences blood vessel structure and blood pressure, the work opens new avenues for thinking about hypertension—particularly in individuals who do not fit the traditional profile of obesity-related cardiovascular disease.
“In the longer term, targeting the molecular pathways uncovered in this study could lead to new strategies aimed at preventing vascular damage and high blood pressure by preserving or restoring healthy fat–vascular communication,” said Dr. Touyz.
About the study
“Ablation of Prdm16 and beige fat identity causes vascular remodeling and elevated blood pressure” was written by Mascha Koenen, Tobias Becher, Giulia Pagano, Ilaria Del Gaudio, Jorge A. Barrero, Augusto C. Montezano, Jenelys Ruiz Ortiz, Zeran Lin, Nicolás Gómez-Banoy, Rose Amblard, Daniel Schriever, Meltem E. Kars, Luisa Rubinelli, Sarah J. Halix, Zhen Fang Huang Cao, Xing Zeng, Scott D. Butler, Yuval Itan, Rhian M. Touyz, Annarita Di Lorenzo, and Paul Cohen. It was published in Science, January 15, 2026, Vol 391, Issue 6782, pp. 306–313.