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Building in resistance to endothelial cell death

Nature Genetics volume 39, pages 1308–1309 (2007)Cite this article

A new study in zebrafish shows that Birc2, a member of the inhibitor of apoptosis (IAP) family, is required for endothelial cell survival. This discovery highlights an important in vivo function of this molecule and suggests potential avenues for the development of new antiangiogenic therapies.

Death is rarely welcome, but inducing the death of blood vessels, especially if there are too many of them, has become a promising strategy to treat cancer patients and prevent blindness. Antiangiogenic agents that inhibit the formation of new blood vessels also act by causing vessel death1. However, many cancer patients are refractory to such antiangiogenic medicine, and others become resistant during treatment1. Thus, identifying new survival or death signals for blood vessels offers opportunities to improve antiangiogenic therapy. Using an elegant series of genetic studies in zebrafish, Santoro et al.2, reporting on page 1397 of this issue, discovered that Birc2 (also termed cIap1 or IAP1), an inhibitor of apoptosis, is critical for the survival of endothelial cells, which line the inner portion of blood vessels. Apart from the relevance of these findings for improving understanding of vascular development, they may create new opportunities for further development of antiangiogenic drug therapies.

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Figure 1: Birc2 regulates endothelial cell survival.

Kim Caesar

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Authors and Affiliations

  1. Massimiliano Mazzone, Carmen Ruiz de Almodovar and Peter Carmeliet are at the Center for Transgene Technology and Gene Therapy, Flanders Institute for Biotechnology (VIB), Katholieke Universiteit Leuven (K.U. Leuven), 3000, Leuven, Belgium. peter.carmeliet@med.kuleuven.be,

    Massimiliano Mazzone, Carmen Ruiz de Almodovar & Peter Carmeliet

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  1. Massimiliano Mazzone
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  2. Carmen Ruiz de Almodovar
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  3. Peter Carmeliet
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Mazzone, M., de Almodovar, C. & Carmeliet, P. Building in resistance to endothelial cell death. Nat Genet 39, 1308–1309 (2007). https://doi.org/10.1038/ng1107-1308

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