The Effects of Resveratrol in Patients with Cardiovascular Disease and Heart Failure: A Narrative Review

Dyck, Garrison J B; Raj, Pema; Zieroth, Shelley; Dyck, Jason R.B.; Ezekowitz, Justin A.

doi:10.3390/ijms20040904

Cited by 143 publications

(100 citation statements)

References 148 publications

(230 reference statements)

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“…Decreased apoptosis and increased autophagy Rat H9c2 cardiomyoblasts [94] questionable. However, resveratrol has been implicated as a cardioprotective drug for many cardiovascular diseases both in preclinical studies [121] and in man [122], and this is thought to be largely due to its anti-inflammatory and anti-oxidant action [123]. Of specific interest for the topic of this review, resveratrol has been shown to lead to activation of AMPK and to reduce cardiac fibrosis and hypertrophy in a mouse model of pressure overload by transverse aortic constriction [124].…”

Section: Resveratrolmentioning

confidence: 99%

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Timm

Tyler

2020

Cardiovasc Drugs Ther

126

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Doxorubicin is a commonly used chemotherapeutic agent for the treatment of a range of cancers, but despite its success in improving cancer survival rates, doxorubicin is cardiotoxic and can lead to congestive heart failure. Therapeutic options for this patient group are limited to standard heart failure medications with the only drug specific for doxorubicin cardiotoxicity to reach FDA approval being dexrazoxane, an iron-chelating agent targeting oxidative stress. However, dexrazoxane has failed to live up to its expectations from preclinical studies while also bringing up concerns about its safety. Despite decades of research, the molecular mechanisms of doxorubicin cardiotoxicity are still poorly understood and oxidative stress is no longer considered to be the sole evil. Mitochondrial impairment, increased apoptosis, dysregulated autophagy and increased fibrosis have also been shown to be crucial players in doxorubicin cardiotoxicity. These cellular processes are all linked by one highly conserved intracellular kinase: adenosine monophosphate-activated protein kinase (AMPK). AMPK regulates mitochondrial biogenesis via PGC1α signalling, increases oxidative mitochondrial metabolism, decreases apoptosis through inhibition of mTOR signalling, increases autophagy through ULK1 and decreases fibrosis through inhibition of TGFβ signalling. AMPK therefore sits at the control point of many mechanisms shown to be involved in doxorubicin cardiotoxicity and cardiac AMPK signalling itself has been shown to be impaired by doxorubicin. In this review, we introduce different agents known to activate AMPK (metformin, statins, resveratrol, thiazolidinediones, AICAR, specific AMPK activators) as well as exercise and dietary restriction, and we discuss the existing evidence for their potential role in cardioprotection from doxorubicin cardiotoxicity.

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Section: Resveratrolmentioning

confidence: 99%

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Timm

Tyler

2020

Cardiovasc Drugs Ther

126

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“…RSV has gained much interest due to its potential to generate a range of therapeutic effects and the suggestion that it is a contributing factor in the so-called "French paradox": the observed reduced risk of coronary artery disease in French people attributed at least in part to the regular consumption of red wine [2]. There is good evidence for RSV supporting the heart function, protecting against cardiovascular diseases [3], neuro-disorders [4,5], diabetes [6], and cancer [7], due to its antioxidant and anti-inflammatory effects. Of particular relevance to this article, RSV has demonstrated a potential for antiaging effects and for protecting against UV damage in the skin due to its antioxidant and collagen stimulating activity [8,9].…”

Section: Introductionmentioning

confidence: 99%

Novel Nanocarriers for Targeted Topical Skin Delivery of the Antioxidant Resveratrol

et al. 2020

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Resveratrol (RSV) is a potent lipophilic antioxidant with a low aqueous solubility. Novel nanoformulations have been successfully developed and evaluated to increase the potential of resveratrol as a skin targeting antioxidant. Nanoformulations were prepared using a spontaneous emulsification method, and characterized and evaluated for their capabilities to penetrate/permeate the skin. In nanoformulations, the thermodynamic activity of the RSV penetration into/permeation through the skin was correlated with the thermodynamic activity of the RSV in the formulations. When terpenes were incorporated into the nanoformulations, the permeation of RSV through the skin increased and correlated with an increasing lipophilicity of the terpene. The nanoemulsion containing eugenol showed the highest RSV penetration into the stratum corneum (SC) and the epidermis-dermis-follicle region, whereas the limonene containing nanoemulsion had the highest RSV permeation through the skin (the enhancement ratios, compared to a saturated solution of RSV, were (i) 9.55 and (ii) 12.61, respectively, based on the average RSV amount (i) in each skin region and (ii) permeation through skin).

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“…The first identified SIRT1 activator was resveratrol, currently used in the treatment of various diseases [19][20][21][22][23][24]. Recent efforts have focused on discovering new synthetic SIRT1-activating compounds (STACs) [25,26].…”

Section: Introductionmentioning

confidence: 99%

Two novel SIRT1 activators, SCIC2 and SCIC2.1, enhance SIRT1-mediated effects in stress response and senescence

et al. 2020

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Nebbioso (2020) Two novel SIRT1 activators, SCIC2 and SCIC2.1, enhance SIRT1-mediated effects in stress response and senescence, Epigenetics, 15:6-7, 664-683, ABSTRACT SIRT1, a NAD + -dependent deacetylase, is the most well-studied member of class III histone deacetylases. Due to its wide range of activities and substrate targets, this enzyme has emerged as a major regulator of different physiological processes. However, SIRT1-mediated alterations are also implicated in the pathogenesis of several conditions, including metabolic and neurodegenerative disorders, and cancer. Current evidence highlights the potential role of SIRT1 as an attractive therapeutic target for disease prevention and treatment strategies, thus propelling the development of new pharmacological agents. By high-throughput screening of a large library of compounds, we identified SCIC2 as an effective SIRT1 activator. This small molecule showed enzymatic activity of 135.8% at 10 μM, an AC 50 value of 50 ± 1.8 µM, and bound SIRT1 with a K D of 26.4 ± 0.6 μM. In order to potentiate its SIRT1-activating ability, SCIC2 was subjected to modelling studies, leading to the identification of a more potent derivative, SCIC2.1. SCIC2.1 displayed higher SIRT1 activity (175%; AC 50 = 36.83 ± 2.23 µM), stronger binding to SIRT1, and greater cell permeability than SCIC2. At cellular level, both molecules did not alter the cell cycle progression of cancer cells and normal cells, and were able to strengthen SIRT1-mediated effects in stress response. Finally, SCIC2 and SCIC2.1 attenuated induction of senescence by reducing senescenceassociated β-galactosidase activity. Our findings warrant further investigation of these two novel SIRT1 activators in in vivo and human studies. ARTICLE HISTORY

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The Effects of Resveratrol in Patients with Cardiovascular Disease and Heart Failure: A Narrative Review

Cited by 143 publications

References 148 publications

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Novel Nanocarriers for Targeted Topical Skin Delivery of the Antioxidant Resveratrol

Two novel SIRT1 activators, SCIC2 and SCIC2.1, enhance SIRT1-mediated effects in stress response and senescence

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