VEGF (vascular endothelial growth factor) is well known as an important molecule in angiogenesis. Its inhibition is pursued as an anticancer therapy; its enhancement as therapy for tissue ischaemia. In the present paper, its role in skeletal muscle is explored, both at rest and after exercise. Muscle VEGF mRNA and protein are increased severalfold after heavy exercise. Whereas global VEGF knockout is embryonically lethal, muscle-specific knockout is not, providing models for studying its functional significance. Its deletion in adult mouse skeletal muscle: (i) reduces muscle capillarity by more than 50%, (ii) decreases exercise endurance time by approximately 80%, and (iii) abolishes the angiogenic response to exercise training. What causes VEGF to increase with exercise is not clear. Despite regulation by HIF (hypoxia-inducible factor), increased HIF on exercise, and PO2 falling to single digit values during exercise, muscle-specific HIF knockout does not impair performance or capillarity, leaving many unanswered questions.
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December 2011
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Conference Article|
November 21 2011
The critical role of VEGF in skeletal muscle angiogenesis and blood flow
Peter D. Wagner
Peter D. Wagner
1
1Distinguished Professor of Medicine and Bioengineering, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, DEPT 0623A, La Jolla, CA 92093-0623, U.S.A.
1email pdwagner@ucsd.edu
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Publisher: Portland Press Ltd
Received:
July 08 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (6): 1556–1559.
Article history
Received:
July 08 2011
Citation
Peter D. Wagner; The critical role of VEGF in skeletal muscle angiogenesis and blood flow. Biochem Soc Trans 1 December 2011; 39 (6): 1556–1559. doi: https://doi.org/10.1042/BST20110646
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