http://link.springer.com/article/10.1007/s10456-016-9535-4
- Cite this article as:
- Núñez-Gómez, E., Pericacho, M., Ollauri-Ibáñez, C. et al. Angiogenesis (2016). doi:10.1007/s10456-016-9535-4
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Abstract
Following
arterial occlusion, blood vessels respond by forming a new network of
functional capillaries (angiogenesis), by reorganizing preexisting
capillaries through the recruitment of smooth muscle cells to generate
new arteries (arteriogenesis) and by growing and remodeling preexisting
collateral arterioles into physiologically relevant arteries (collateral
development). All these processes result in the recovery of organ
perfusion. The importance of endoglin in post-occlusion reperfusion is
sustained by several observations: (1) endoglin expression is increased
in vessels showing active angiogenesis/remodeling; (2) genetic endoglin
haploinsufficiency in humans causes deficient angiogenesis; and (3) the
reduction of endoglin expression by gene disruption or the
administration of endoglin-neutralizing antibodies reduces angiogenesis
and revascularization. However, the precise role of endoglin in the
several processes associated with revascularization has not been
completely elucidated and, in some cases, the function ascribed to
endoglin by different authors is controversial. The purpose of this
review is to organize in a critical way the information available for
the role of endoglin in several phenomena (angiogenesis, arteriogenesis
and collateral development) associated with post-ischemic
revascularization.
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