Angiogenesis: focusing on the effects of exercise in aging and cancer

Kwak, Seong-Eun; Lee, Ji‐Hyun; Zhang, Didi; Song, Wook

doi:10.20463/jenb.2018.0020

Cited by 30 publications

(29 citation statements)

References 48 publications

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“…Exercise induces angiogenesis. Aging is accompanied by diminished angiogenesis in endothelial cells and muscle tissues and, hence, lower levels of angiogenic factors (Kwak, Lee, Zhang, & Song, ). Exercise promotes angiogenesis by increasing shear stress in vasculature and by up‐regulating VEGF (Garza et al, ).…”

Section: Molecular Basis Of Resveratrol Actionmentioning

confidence: 99%

Pharmacological basis and new insights of resveratrol action in the cardiovascular system

Cheng

Luo

Lau

et al. 2019

British J Pharmacology

113

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Resveratrol (trans‐3,4′,5‐trihydroxystilbene) belongs to the family of natural phytoalexins. Resveratrol first came to our attention in 1992, following reports of the cardioprotective effects of red wine. Thereafter, resveratrol was shown to exert antioxidant, anti‐inflammatory, anti‐proliferative, and angio‐regulatory effects against atherosclerosis, ischaemia, and cardiomyopathy. This article critically reviews the current findings on the molecular basis of resveratrol‐mediated cardiovascular benefits, summarizing the broad effects of resveratrol on longevity regulation, energy metabolism, stress resistance, exercise mimetics, circadian clock, and microbiota composition. In addition, this article also provides an update, both preclinically and clinically, on resveratrol‐induced cardiovascular protection and discusses the adverse and inconsistent effects of resveratrol reported in both preclinical and clinical studies. Although resveratrol has been claimed as a master anti‐aging agent against several age‐associated diseases, further detailed mechanistic investigation is still required to thoroughly unravel the therapeutic value of resveratrol against cardiovascular diseases at different stages of disease development. Linked Articles This article is part of a themed section on The Pharmacology of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.6/issuetoc

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Section: Molecular Basis Of Resveratrol Actionmentioning

confidence: 99%

Pharmacological basis and new insights of resveratrol action in the cardiovascular system

Cheng

Luo

Lau

et al. 2019

British J Pharmacology

113

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“…Structural and functional decline of the skeletal muscle occurs with aging 23,24 . Aging compromises skeletal muscle circulation as well as blunts the angiogenic properties of this tissue 25,26 . Impaired microvascular functions perturb myogenic cell homeostasis, limit nitric oxide (NO) activity, increase production of vasoconstrictor factors, and is associated with inflammationrelated oxidative stress 27,28 .…”

Section: Discussionmentioning

confidence: 99%

Urolithin A augments angiogenic pathways in skeletal muscle by bolstering NAD+ and SIRT1

Ghosh

Das

Biswas

et al. 2020

Sci Rep

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Urolithin A (UA) is a natural compound that is known to improve muscle function. In this work we sought to evaluate the effect of UA on muscle angiogenesis and identify the underlying molecular mechanisms. C57BL/6 mice were administered with UA (10 mg/body weight) for 12–16 weeks. ATP levels and NAD+ levels were measured using in vivo 31P NMR and HPLC, respectively. UA significantly increased ATP and NAD+ levels in mice skeletal muscle. Unbiased transcriptomics analysis followed by Ingenuity Pathway Analysis (IPA) revealed upregulation of angiogenic pathways upon UA supplementation in murine muscle. The expression of the differentially regulated genes were validated using quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Angiogenic markers such as VEGFA and CDH5 which were blunted in skeletal muscles of 28 week old mice were found to be upregulated upon UA supplementation. Such augmentation of skeletal muscle vascularization was found to be bolstered via Silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1-alpha (PGC-1α) pathway. Inhibition of SIRT1 by selisistat EX527 blunted UA-induced angiogenic markers in C2C12 cells. Thus this work provides maiden evidence demonstrating that UA supplementation bolsters skeletal muscle ATP and NAD+ levels causing upregulated angiogenic pathways via a SIRT1-PGC-1α pathway.

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“…Angiogenesis refers to the growth of new blood vessels from original vessels during natural development, reproduction, or tissue repair [52]. Angiogenesis is linked to exercise, aging, and cancer [53,54]. Angiogenic factors are regulated by vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and hypoxia-inducible factors (HIFs).…”

Section: High-intensity Exercise/training and Skeletal Muscle Angiogementioning

confidence: 99%

“…Exercise induces a range of adaptations, including an upregulation of angiogenesis that, in turn contributes to exercise adaptations [54]. Several studies have evaluated changes associated with angiogenesis after exercise.…”

Section: High-intensity Exercise/training and Skeletal Muscle Angiogementioning

confidence: 99%

The Molecular Adaptive Responses of Skeletal Muscle to High-Intensity Exercise/Training and Hypoxia

Atakan

et al. 2020

Antioxidants

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High-intensity exercise/training, especially interval exercise/training, has gained popularity in recent years. Hypoxic training was introduced to elite athletes half a century ago and has recently been adopted by the general public. In the current review, we have summarised the molecular adaptive responses of skeletal muscle to high-intensity exercise/training, focusing on mitochondrial biogenesis, angiogenesis, and muscle fibre composition. The literature suggests that (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) PGC-1α, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor 1-alpha (HIF1-α) might be the main mediators of skeletal muscle adaptations to high-intensity exercises in hypoxia. Exercise is known to be anti-inflammatory, while the effects of hypoxia on inflammatory signalling are more complex. The anti-inflammatory effects of a single session of exercise might result from the release of anti-inflammatory myokines and other cytokines, as well as the downregulation of Toll-like receptor signalling, while training-induced anti-inflammatory effects may be due to reductions in abdominal and visceral fat (which are main sources of pro-inflammatory cytokines). Hypoxia can lead to inflammation, and inflammation can result in tissue hypoxia. However, the hypoxic factor HIF1-α is essential for preventing excessive inflammation. Disease-induced hypoxia is related to an upregulation of inflammatory signalling, but the effects of exercise-induced hypoxia on inflammation are less conclusive. The effects of high-intensity exercise under hypoxia on skeletal muscle molecular adaptations and inflammatory signalling have not been fully explored and are worth investigating in future studies. Understanding these effects will lead to a more comprehensive scientific basis for maximising the benefits of high-intensity exercise.

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Angiogenesis: focusing on the effects of exercise in aging and cancer

Cited by 30 publications

References 48 publications

Pharmacological basis and new insights of resveratrol action in the cardiovascular system

Pharmacological basis and new insights of resveratrol action in the cardiovascular system

Urolithin A augments angiogenic pathways in skeletal muscle by bolstering NAD+ and SIRT1

The Molecular Adaptive Responses of Skeletal Muscle to High-Intensity Exercise/Training and Hypoxia

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