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Dysregulated exocytosis of angiopoietin-2 drives cerebral cavernous malformation

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A new study has proposed a mechanism for the pathogenesis of cerebral cavernous malformation (CCM) that links endothelial CCM3 deficiency to increased secretion of the vascular destabilizing protein angiopoietin-2 (ANGPT2).

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Figure 1: The pathogenesis of CCM3-associated cerebral cavernous malformation.

Marina Corral Spence/Nature Publishing Group

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Author information

Authors and Affiliations

  1. Helong Zhao and Tara M. Mleynek are in the Molecular Medicine Program, School of Medicine, University of Utah, Salt Lake City, Utah, USA.,

    Helong Zhao & Tara M Mleynek

  2. Dean Y. Li is at the School of Medicine and Health Sciences, University of Utah, Salt Lake City, Utah, USA.,

    Dean Y Li

Authors
  1. Helong Zhao
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  2. Tara M Mleynek
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  3. Dean Y Li
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Corresponding author

Correspondence to Dean Y Li.

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Competing interests

D.Y.L. is cofounder of the biotechnology companies Navigen and Recursion Pharmaceuticals.

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Zhao, H., Mleynek, T. & Li, D. Dysregulated exocytosis of angiopoietin-2 drives cerebral cavernous malformation. Nat Med 22, 971–973 (2016). https://doi.org/10.1038/nm.4178

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