Published on: Jan 15, 2026
In 2015, Paul Cohen founded Rockefeller University’s Weslie R. and William H. Janeway Laboratory of Molecular Metabolism with a central mission: to uncover the precise biological mechanisms through which obesity leads to disease. Since then, the lab has generated pivotal insights into how adipose tissue communicates with other organs, revealed protective roles of brown and beige fat, and opened new avenues for therapies aimed at creating metabolically healthier fat to disrupt the link between obesity and chronic disease.
In a recent breakthrough Cohen and his team identified a direct biological mechanism connecting adipose tissue to hypertension. Their work shows that the loss of beige fat a brown fat–like tissue in adults activates the enzyme QSOX1, leading to vascular stiffening and heightened sensitivity to blood pressure–raising signals. This discovery highlights that fat quality, not just fat quantity, plays a critical role in cardiovascular health and points toward new precision-based therapeutic strategies.
The team emphasizes that uncovering this mechanism required a multidisciplinary approach. Obesity-related hypertension is influenced by multiple factors, including aging, making it difficult to disentangle cause and effect. By focusing on the molecular changes within fat tissue itself, the researchers identified disease pathways that extend beyond obesity alone offering potential treatments even for individuals who are not obese.
Their findings also underscore the promise of personalized medicine. Understanding the molecular drivers of hypertension could move treatment beyond one-size-fits-all approaches toward interventions tailored to an individual’s biological profile.
Mechanistically, the study demonstrated that removing beige fat from otherwise healthy mice caused hypertension, vascular remodeling, fibrosis, and exaggerated vasoconstrictive responses. Importantly, deleting QSOX1 prevented these effects, identifying the enzyme as a potential therapeutic target.
Looking ahead, Cohen’s lab is exploring whether existing FDA-approved drugs influence brown fat activity, raising the possibility of drug repurposing. The team is also extending their work into human studies, using genetic and imaging data to better understand brown fat function in people.
This research was guided by a “reverse translation” approach starting with large clinical observations and then validating mechanisms in experimental models. Leveraging a unique dataset of over 100,000 patients from Memorial Sloan Kettering, whose scans incidentally revealed brown fat, the team was able to correlate brown fat presence with cardiometabolic health outcomes. This unprecedented dataset continues to fuel discoveries at the intersection of metabolism, vascular biology, and aging.
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