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Michael Potente’s laboratory focuses on the regulation of blood vessel growth (angiogenesis) by metabolism. Angiogenesis and metabolism are tightly coupled as blood vessels supply nutrients and oxygen to energy-consuming tissues (e.g. brain, heart or skeletal muscle). A reduction in tissue oxygen tension or nutrient availability is a primary stimulus for angiogenesis, which prompts endothelial cells (ECs) to become motile, invasive and to form new vessel connections. His group studies how ECs sense such environmental signals and how they use this information to build vascular networks of organ-specific size, shape and density. They are also interested in the metabolism of ECs, aiming to understand how endothelial metabolic state controls vessel growth and function, and how deregulation contributes to disease. The forkhead box O (FOXO) family of transcription factors have been shown to control cell proliferation, metabolism, and stress resistance (Oellerich and Potente, 2012). FOXOs are key transcriptional effectors of the PI3K / AKT pathway that coordinates growth and metabolism in normal and cancer cells. PI3K signalling inhibits FOXO activity through AKT-mediated phosphorylation leading to the exclusion of FOXOs from the nucleus. Previous work from the Potente laboratory has shown that FOXOs suppress endothelial angiogenic behaviour in surrogate assays of angiogenesis (Potente et al., 2005). However, the specific cellular functions of FOXOs in angiogenesis in vivo remain unclear. Michael Potente uses a combination of genetic, biochemical and imaging technologies to define the role of individual FOXO family members for endothelial growth and metabolism in models of vascular development, homeostasis and disease.