Generic Work

 

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer. Publique Deposited

Contenu téléchargeable

Télécharger le PDF

MLA citation style

Gutkind, J. Silvio, Doci, Colleen L, and Sakurai, Atsuko. Semaphorin Signaling In Angiogenesis, Lymphangiogenesis and Cancer. Nature Publishing Group. 2012. https://mushare.marian.edu/concern/generic_works/6bc7367b-80af-4656-8710-29cde66be2a9?locale=fr

APA citation style

Gutkind, J. Silvio, Doci, Colleen L, & Sakurai, Atsuko. (2012). Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer. https://mushare.marian.edu/concern/generic_works/6bc7367b-80af-4656-8710-29cde66be2a9?locale=fr

Chicago citation style

Gutkind, J. Silvio, Doci, Colleen L., and Sakurai, Atsuko. Semaphorin Signaling In Angiogenesis, Lymphangiogenesis and Cancer. Nature Publishing Group. 2012. https://mushare.marian.edu/concern/generic_works/6bc7367b-80af-4656-8710-29cde66be2a9?locale=fr

Note: These citations are programmatically generated and may be incomplete.

Angiogenesis, the formation of new blood vessels from preexisting vasculature, is essential for many physiological processes, and aberrant angiogenesis contributes to some of the most prevalent human diseases, including cancer. Angiogenesis is controlled by delicate balance between pro- and anti-angiogenic signals. While pro-angiogenic signaling has been extensively investigated, how developmentally regulated, naturally occurring anti-angiogenic molecules prevent the excessive growth of vascular and lymphatic vessels is still poorly understood. In this review, we summarize the current knowledge on how semaphorins and their receptors, plexins and neuropilins, control normal and pathological angiogenesis, with an emphasis on semaphorin-regulated anti-angiogenic signaling circuitries in vascular and lymphatic endothelial cells. This emerging body of information may afford the opportunity to develop novel anti-angiogenic therapeutic strategies.

Creator
Publisher
Language
Identifier
Mot-clé
Date created
Related URL
Resource type
Source
  • fp_db13
  • Cell research (Vol.22, Iss.1)
Rights statement
License

Relationships

Dans Collection:

Articles