Pengchun Yu

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Lymphatic vessels maintain tissue fluid homeostasis. They also serve as essential conduits for tumor cell dissemination and the removal of cholesterol from the aortic wall. Accordingly, excessive or insufficient lymphangiogenesis (formation of the lymphatic vasculature) underlies the pathogenesis of multiple human diseases such as cancer, lymphedema, and atherosclerosis, for which curative treatments are not available. Thus, a better understanding of the mechanism of lymphangiogenesis may guide the development of new therapeutic strategies.

Our recent study (Yu et al., Nature, 2017) has discovered that a novel cellular mechanism—endothelial glycolysis—plays a crucial role in lymphangiogenesis . Cells convert glucose into pyruvate through glycolytic metabolism, which generates ATP. Lymphatic endothelial cells (LECs) exhibit robust glycolysis and heavily rely on this metabolic process for ATP production. Accordingly, glycolytic inhibition through genetic ablation of a rate-limiting glycolytic enzyme hexokinase 2 (HK2) profoundly impairs lymphatic vessel formation. Importantly, endothelial glycolysis can be enhanced by fibroblast growth factor (FGF)2 signaling via HK2 and is essential for FGF2-driven lymphangiogenesis. Our study highlights the importance of endothelial glycolysis in lymphatic vessel formation. It also indicates that lymphangiogenic signaling controls endothelial metabolism in order to elicit a metabolic state permissive for growth and proliferation.

Research projects of our laboratory are built upon this recent study to further study the crosstalk between metabolic programs and lymphangiogenic signaling events and to understand the involvement of cellular metabolism in the pathogenesis of vascular diseases.

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