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. 2019 Dec 13;8(12):2199. doi: 10.3390/jcm8122199

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Disruption of physiological vasa vasorum contributes to plaque formation. Factors such as diabetes, hypertension and hypercholesteraemia can lead to localised or systemic inflammation and hypoxia driving atherogenic conditions. Formation of adventitial vasa vasorum (VV) occurs in response to the metabolic demand of the outer and medial layers of an artery. Under hypoxic conditions, hypoxia-inducible factor (HIF)-1α and HIF-2α induce vascular endothelial growth factor (VEGF)A, a proangiogenic mediator. Hypoxic conditions also provide favourable conditions for fibroblast growth factor (FGF)2, promoting EC growth and stabilising VV. Additionally, inflammation triggers VV sprouting from the adventitia into the arterial lumen by inducing secretion of several angiogenic growth factors.