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Endothelial cell metabolism in normal and diseased vasculature
#MMPMID25814684
Eelen G
; de Zeeuw P
; Simons M
; Carmeliet P
Circ Res
2015[Mar]; 116
(7
): 1231-44
PMID25814684
show ga
Higher organisms rely on a closed cardiovascular circulatory system with blood
vessels supplying vital nutrients and oxygen to distant tissues. Not
surprisingly, vascular pathologies rank among the most life-threatening diseases.
At the crux of most of these vascular pathologies are (dysfunctional) endothelial
cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable
capability to switch rapidly from a quiescent state to a highly migratory and
proliferative state during vessel sprouting. This angiogenic switch has long been
considered to be dictated by angiogenic growth factors (eg, vascular endothelial
growth factor) and other signals (eg, Notch) alone, but recent findings show that
it is also driven by a metabolic switch in ECs. Furthermore, these changes in
metabolism may even override signals inducing vessel sprouting. Here, we review
how EC metabolism differs between the normal and dysfunctional/diseased
vasculature and how it relates to or affects the metabolism of other cell types
contributing to the pathology. We focus on the biology of ECs in tumor blood
vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial
metabolism in key pathological processes. Finally, current as well as unexplored
EC metabolism-centric therapeutic avenues are discussed.
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