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Review
. 2021 Sep 21;22(18):10152.
doi: 10.3390/ijms221810152.

The Effect of Resveratrol on the Cardiovascular System from Molecular Mechanisms to Clinical Results (VSports app下载)

Roland Gal  1   2 , Laszlo Deres  1   2 , Kalman Toth  1   2 , Robert Halmosi  1   2 , Tamas Habon  1   2
Affiliations
Review

The Effect of Resveratrol on the Cardiovascular System from Molecular Mechanisms to Clinical Results

V体育ios版 - Roland Gal et al. Int J Mol Sci. .

Abstract

Cardiovascular diseases are the leading causes of death worldwide. The cardioprotective effects of natural polyphenols such as resveratrol (3,5,4-trihydroxystilbene) have been extensively investigated throughout recent decades. Many studies of RES have focused on its favorable effects on pathological conditions related to cardiovascular diseases and their risk factors. The aim of this review was to summarize the wide beneficial effects of resveratrol on the cardiovascular system, including signal transduction pathways of cell longevity, energy metabolism of cardiomyocytes or cardiac remodeling, and its anti-inflammatory and antioxidant properties. In addition, this paper discusses the significant preclinical and human clinical trials of recent years with resveratrol on cardiovascular system VSports手机版. Finally, we present a short overview of antiviral and anti-inflammatory properties and possible future perspectives on RES against COVID-19 in cardiovascular diseases. .

Keywords: cardiovascular diseases; heart failure; inflammation; oxidative stress; resveratrol V体育安卓版. .

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Beneficial effects of RES on cardiovascular system. Akt: protein kinase B; AMPK: AMP-activated protein kinase; COX: cyclooxygenase; Drp1: dynamin-related protein 1; GPx: glutathione peroxidase; GSH: glutathione; eNOS: endothelial nitric oxide synthase; HO-1: heme oxygenase-1; ICAM: intracellular cell adhesion molecule; JAK: Janus kinase; MAPK: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; NF-κB: nuclear factor kappa B; NOX: NADPH oxidases; PI3K: phosphatidylinositol 3-kinase; PGC-1α: peroxisome-proliferator-activated receptor gamma coactivator 1-alpha; SOD: superoxide dismutase; STAT: signal transducer and activator of transcription proteins; TGF-β: transforming growth factor; TLR4: toll-like receptor 4; VCAM: vascular cell adhesion molecule. References: [31,32,33,34,35,36,37,38,39,40,41,42,44,45,46,47,55,56,57,59,60,61,62,64,68,69,70,71,73,74,78,79,84,85,86,87,92,94,97,98,100,101,105].
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