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. 2015 Feb 11;6:35. doi: 10.3389/fgene.2015.00035

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Copyright © 2015 Ardelean and Letarte.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Dysregulated angiogenesis in HHT. Normally, when quiescent vessels are activated, they proliferate, migrate and mature until the physiological needs of the organ have been met, and then regress. Pathological angiogenesis commences when the angiogenic–angiostatic balance is disrupted, leading to dysregulated angiogenesis, excessive or reduced tissue MVD and possibly to AVMs. In Eng^+/- and Alk1^+/- models of HHT, an imbalance in the pulmonary angiostatic TSP-1 and vascular destabilizing factor Ang-2 respectively, led to reduced peripheral lung MVD in both models. However, it is unknown if dysregulated angiogenesis is involved in the development of AVMs in HHT. Angiogenic factors; angiostatic proteins.

Inline graphic — Dysregulated angiogenesis in HHT. Normally, when quiescent vessels are activated, they proliferate, migrate and mature until the physiological needs of the organ have been met, and then regress. Pathological angiogenesis commences when the angiogenic–angiostatic balance is disrupted, leading to dysregulated angiogenesis, excessive or reduced tissue MVD and possibly to AVMs. In Eng^+/- and Alk1^+/- models of HHT, an imbalance in the pulmonary angiostatic TSP-1 and vascular destabilizing factor Ang-2 respectively, led to reduced peripheral lung MVD in both models. However, it is unknown if dysregulated angiogenesis is involved in the development of AVMs in HHT. Angiogenic factors; angiostatic proteins.