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Metabolic regulation of exercise-induced angiogenesis

Skeletal muscle relies on an ingenious network of blood vessels, which ensures optimal oxygen and nutrient supply. An increase in muscle vascularization is an early adaptive event to exercise training, but the cellular and molecular mechanisms underlying exercise-induced blood vessel formation are n...

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Detalles Bibliográficos
Autores principales: Gorski, Tatiane, De Bock, Katrien
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439921/
https://www.ncbi.nlm.nih.gov/pubmed/32923947
http://dx.doi.org/10.1530/VB-19-0008
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author Gorski, Tatiane
De Bock, Katrien
author_facet Gorski, Tatiane
De Bock, Katrien
author_sort Gorski, Tatiane
collection PubMed
description Skeletal muscle relies on an ingenious network of blood vessels, which ensures optimal oxygen and nutrient supply. An increase in muscle vascularization is an early adaptive event to exercise training, but the cellular and molecular mechanisms underlying exercise-induced blood vessel formation are not completely clear. In this review, we provide a concise overview on how exercise-induced alterations in muscle metabolism can evoke metabolic changes in endothelial cells (ECs) that drive muscle angiogenesis. In skeletal muscle, angiogenesis can occur via sprouting and splitting angiogenesis and is dependent on vascular endothelial growth factor (VEGF) signaling. In the resting muscle, VEGF levels are controlled by the estrogen-related receptor γ (ERRγ). Upon exercise, the transcriptional coactivator peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC1α) orchestrates several adaptations to endurance exercise within muscle fibers and simultaneously promotes transcriptional activation of Vegf expression and increased muscle capillary density. While ECs are highly glycolytic and change their metabolism during sprouting angiogenesis in development and disease, a similar role for EC metabolism in exercise-induced angiogenesis in skeletal muscle remains to be elucidated. Nonetheless, recent studies have illustrated the importance of endothelial hydrogen sulfide and sirtuin 1 (SIRT1) activity for exercise-induced angiogenesis, suggesting that EC metabolic reprogramming may be fundamental in this process. We hypothesize that the exercise-induced angiogenic response can also be modulated by metabolic crosstalk between muscle and the endothelium. Defining the underlying molecular mechanisms responsible for skeletal muscle angiogenesis in response to exercise will yield valuable insight into metabolic regulation as well as the determinants of exercise performance.
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spelling pubmed-74399212020-09-10 Metabolic regulation of exercise-induced angiogenesis Gorski, Tatiane De Bock, Katrien Vasc Biol Mini Review Skeletal muscle relies on an ingenious network of blood vessels, which ensures optimal oxygen and nutrient supply. An increase in muscle vascularization is an early adaptive event to exercise training, but the cellular and molecular mechanisms underlying exercise-induced blood vessel formation are not completely clear. In this review, we provide a concise overview on how exercise-induced alterations in muscle metabolism can evoke metabolic changes in endothelial cells (ECs) that drive muscle angiogenesis. In skeletal muscle, angiogenesis can occur via sprouting and splitting angiogenesis and is dependent on vascular endothelial growth factor (VEGF) signaling. In the resting muscle, VEGF levels are controlled by the estrogen-related receptor γ (ERRγ). Upon exercise, the transcriptional coactivator peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC1α) orchestrates several adaptations to endurance exercise within muscle fibers and simultaneously promotes transcriptional activation of Vegf expression and increased muscle capillary density. While ECs are highly glycolytic and change their metabolism during sprouting angiogenesis in development and disease, a similar role for EC metabolism in exercise-induced angiogenesis in skeletal muscle remains to be elucidated. Nonetheless, recent studies have illustrated the importance of endothelial hydrogen sulfide and sirtuin 1 (SIRT1) activity for exercise-induced angiogenesis, suggesting that EC metabolic reprogramming may be fundamental in this process. We hypothesize that the exercise-induced angiogenic response can also be modulated by metabolic crosstalk between muscle and the endothelium. Defining the underlying molecular mechanisms responsible for skeletal muscle angiogenesis in response to exercise will yield valuable insight into metabolic regulation as well as the determinants of exercise performance. Bioscientifica Ltd 2019-03-11 /pmc/articles/PMC7439921/ /pubmed/32923947 http://dx.doi.org/10.1530/VB-19-0008 Text en © 2019 The authors http://creativecommons.org/licenses/by-nc/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) .
spellingShingle Mini Review
Gorski, Tatiane
De Bock, Katrien
Metabolic regulation of exercise-induced angiogenesis
title Metabolic regulation of exercise-induced angiogenesis
title_full Metabolic regulation of exercise-induced angiogenesis
title_fullStr Metabolic regulation of exercise-induced angiogenesis
title_full_unstemmed Metabolic regulation of exercise-induced angiogenesis
title_short Metabolic regulation of exercise-induced angiogenesis
title_sort metabolic regulation of exercise-induced angiogenesis
topic Mini Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439921/
https://www.ncbi.nlm.nih.gov/pubmed/32923947
http://dx.doi.org/10.1530/VB-19-0008
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