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Invited review: activity-induced angiogenesis

  • Cardiovascular Physiology
  • Published:
Pflügers Archiv - European Journal of Physiology Aims and scope Submit manuscript

Abstract

The dynamic biochemical and mechanical environment around blood vessels during muscle activity generates powerful stimuli for vascular remodelling. Ultimately, this must lead to a coordinated expansion of various elements of the cardiovascular system in order to support enhanced aerobic exercise. Vascular endothelial growth factor plays a central role, and understanding how this is regulated in vivo by changes in transcription and stability of mRNA, production of protein and interaction with other growth factors, is a continuing challenge. Exercise hyperaemia leads to an increase in microvascular shear stress, which stimulates endothelial release of nitric oxide, whilst proteolytic modification of the extracellular matrix is induced by mechanical deformation during cyclical contractions or muscle overload. These components of the exercise response lead to different forms of capillary growth, and subsequent expansion of the microcirculation may not have the same functional outcome. In vitro and in vivo studies have shown a complex interplay between different cytokines, receptors and mural cells in directing the necessary tissue re-organisation. The mechanisms involved in arteriogenesis are less well-understood than those of angiogenesis, but application of these data to understanding vascular remodelling in response to exercise may help resolve a range of cardiovascular dysfunction.

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Abbreviations

Ang:

angiopoietin

C:F:

numerical capillary to fibre ratio

CD:

capillary density

CHF:

chronic (congestive) heart failure

EC:

endothelial cells

ECM:

extracellular matrix

eNOS:

endothelial nitric oxide synthase

EPC:

endothelial progenitor cells

FGF:

fibroblast growth factor

HIF:

hypoxia-inducible factor

MO2max :

maximal oxygen consumption

MMP:

matrix metalloproteinases

NOS:

nitric oxide synthase

PDGF:

platelet-derived growth factor

PGI2 :

prostacyclin

PlGF:

placental growth factor

RTK:

receptor tyrosine kinase

TGF:

transforming growth factor

TIMPs:

tissue inhibitors of matrix metalloproteinases

VEGF:

vascular endothelial growth factor

VEGFR:

VEGF receptor

VSM:

vascular smooth muscle

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Egginton, S. Invited review: activity-induced angiogenesis. Pflugers Arch - Eur J Physiol 457, 963–977 (2009). https://doi.org/10.1007/s00424-008-0563-9

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