Targeting GPR116 (Adgrf5) to preserve endothelial identity and restore thermogenic fat function
© Georgiadi/Herzig
Brown adipose tissue (BAT) relies on a dense vascular network to support its high metabolic activity. While blood vessels are known to supply oxygen and nutrients, it remains unclear how endothelial cells sense changing physiological demands and coordinate tissue remodeling. This project investigates the role of the adhesion GPCR GPR116 (Adgrf5) as an endothelial mechanosensor that detects blood-flow-derived signals and regulates communication between blood vessels and adipose tissue. We aim to understand how impaired flow sensing contributes to vascular dysfunction and thermogenic decline during ageing, obesity, and thermoneutrality, and whether restoring GPR116 signaling can preserve endothelial identity and reactivate thermogenic fat function.
Project Leaders
Anastasia Georgiadi Ph.D.
Junior Group Leader: Endocrine Pharmcology (ENP), Institute of Diabetes and Cancer (IDC)
Ingolstädter Langstraße 1
85764 Neuherberg
© Michael Haggenmüller
Prof. Stephan Herzig Ph.D.
Professor and Research Director Helmholtz Munich
Ingolstädter Landstraße 1
85764 Neuherberg
Head of Department
Helmholtz Diabetes Center HDC
Joint Heidelberg-IDC Translational Diabetes Unit Heidelberg University Hospital
© Jan Roeder