Incomplete and transitory decrease of glycolysis: A new paradigm for anti-angiogenic therapy?

Sandra Schoors, Anna Rita Cantelmo, Maria Georgiadou, Peter Stapor, Xingwu Wang, Annelies Quaegebeur, Sandra Cauwenberghs, Brian W. Wong, Francesco Bifari, Ilaria Decimo, Luc Schoonjans, Katrien De Bock, Mieke Dewerchin, Peter Carmeliet

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


During vessel sprouting, a migratory endothelial tip cell guides the sprout, while proliferating stalk cells elongate the branch. Tip and stalk cell phenotypes are not genetically predetermined fates, but are dynamically interchangeable to ensure that the fittest endothelial cell (EC) leads the vessel sprout. ECs increase glycolysis when forming new blood vessels. Genetic deficiency of the glycolytic activator PFKFB3 in ECs reduces vascular sprouting by impairing migration of tip cells and proliferation of stalk cells. PFKFB3-driven glycolysis promotes the tip cell phenotype during vessel sprouting, since PFKFB3 overexpression overrules the pro-stalk activity of Notch signaling. Furthermore, PFKFB3-deficient ECs cannot compete with wild-type neighbors to form new blood vessels in chimeric mosaic mice. In addition, pharmacological PFKFB3 blockade reduces pathological angiogenesis with modest systemic effects, likely because it decreases glycolysis only partially and transiently.

Original languageEnglish
Pages (from-to)16-22
Number of pages7
JournalCell Cycle
Issue number1
StatePublished - Jan 1 2014


  • Angiogenesis
  • Endothelial cell
  • Glycolysis
  • Metabolism
  • Vessel sprouting


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