Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 RSV is a possible therapeutic option for patients with CKD with or without CVD. In this regard, RSV can influence the traditional and nontraditional CVD risk factors and alleviate the effects of uremic toxins in patients with CKD.
Cai-Mei Zheng
 + 1795 word(s) 1795 2020-08-31 14:34:35 |
2 format correction
Peter Tang
 -53 word(s) 1742 2020-10-25 05:26:03 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Song, J.; Shen, T.; Hou, Y.; Chang, J.; Lu, C.; Liu, W.; Chen, P.; Chen, B.; Zheng, C.; Lu, K. Resveratrol on the Cardiovascular Health. Encyclopedia. Available online: https://encyclopedia.pub/entry/2771 (accessed on 17 November 2024).
Song J, Shen T, Hou Y, Chang J, Lu C, Liu W, et al. Resveratrol on the Cardiovascular Health. Encyclopedia. Available at: https://encyclopedia.pub/entry/2771. Accessed November 17, 2024.
Song, Jenn-Yeu, Ta-Chung Shen, Yi-Chou Hou, Jia-Feng Chang, Chien-Lin Lu, Wen-Chih Liu, Po-Jui Chen, Bo-Hau Chen, Cai-Mei Zheng, Kuo-Cheng Lu. "Resveratrol on the Cardiovascular Health" Encyclopedia, https://encyclopedia.pub/entry/2771 (accessed November 17, 2024).
Song, J., Shen, T., Hou, Y., Chang, J., Lu, C., Liu, W., Chen, P., Chen, B., Zheng, C., & Lu, K. (2020, October 23). Resveratrol on the Cardiovascular Health. In Encyclopedia. https://encyclopedia.pub/entry/2771
Song, Jenn-Yeu, et al. "Resveratrol on the Cardiovascular Health." Encyclopedia. Web. 23 October, 2020.
Resveratrol on the Cardiovascular Health
Edit
This entry is adapted from the peer-reviewed paper 10.3390/ijms21176294

Cardiovascular disease (CVD) is closely related to chronic kidney disease (CKD), and patients with CKD have a high risk of CVD-related mortality. Traditional CVD risk factors cannot account for the higher cardiovascular risk of patients with CKD, and standard CVD interventions cannot reduce the mortality rates among patients with CKD. Nontraditional factors related to mineral and vitamin-D metabolic disorders provide some explanation for the increased CVD risk. Non-dialyzable toxins, indoxyl sulfate (IS) and p-cresol sulfate (PCS)—produced in the liver by colonic microorganisms—cause kidney and vascular dysfunction. Plasma trimethylamine-N-oxide (TMAO)—a gut microbe-dependent metabolite of dietary L-carnitine and choline—is elevated in CKD and related to vascular disease, resulting in poorer long-term survival. Therefore, the modulation of colonic flora can improve prospects for patients with CKD. Managing metabolic syndrome, anemia, and abnormal mineral metabolism is recommended for the prevention of CVD in patients with CKD. Considering nontraditional risk factors, the use of resveratrol (RSV), a nutraceutical, can be helpful for patients with CVD and CKD. Resveratrol is a possible therapeutic option for patients with CKD with or without CVD. In this regard, RSV can influence the traditional and nontraditional CVD risk factors and alleviate the effects of uremic toxins in patients with CKD.

resveratrol, CKD, CVD, uremic toxin

1. Introduction 

Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). The strong causality between CKD and CVD risk means that preventing the progression of CKD can also prevent CVD. In patients with CKD, increased CVD risk is multifactorial, and a targeted intervention for a single traditional risk factor is inadequate. Therefore, research on innovative therapeutic strategies and CVD risk factors is essential [1]. We evaluated traditional and nontraditional risk factors of CVD in CKD and analyzed their relationship. Nutraceuticals are derived from foods and have been demonstrated to have physiological benefits, establishing them as likely the most suitable option for preventing CVD in patients with CKD.

Resveratrol (RSV), a nutraceutical, is a naturally occurring polyphenol that can be found in red wine and grapes [2]. Reports have indicated that it is beneficial for treating or preventing CVD by improving metabolic syndrome components [3][4]. Moreover, RSV reduces the amount of plasma protein-bound uremic toxins and trimethylamine-N-oxide (TMAO) levels by maintaining balance in the gut microbiota [5]. RSV has been demonstrated to be safe and tolerable in humans. This overview focuses on how RSV can influence traditional and nontraditional cardiovascular risk factors and provide beneficial effects by attenuating the effect of uremic toxins in patients with CKD.

2.  Relationship between CVD and CKD

The traditional risk factors common for CVD and CKD are advanced age, hypertension, diabetes, dyslipidemia, smoking habit, family history of CVD or CKD and male sex. Toxic metabolites produced during uremia, such as indoxyl sulfate (IS), account for most cases of CVD in patients with CKD. Changes in how these chemicals are metabolized constitute nontraditional risk factors [6][7]. Other nontraditional factors, including TMAO, accumulate in patients with CKD and aggravate CVD. In addition, dysregulation of calcium, phosphorus, PTH or vitamin D metabolism was evaluated.

Screening and testing in the early stages of CKD can aid the development of interventions that can delay disease progression. In fact, the focus of treatments and interventions should be shifted to the early stage of CKD because early identification through screening may substantially attenuate the impact of CKD and delay or even prevent its development [8].

3.  Effect of Nontraditional Risk Factors (Uremic Toxins) on the Development of Cardiovascular Disease

In patients with CKD, CVD is highly prevalent and traditional risk factors cannot adequately predict cardiovascular events. In CKD, the influx of urea and other residual toxins alters the gut microbiota. The number of beneficial microbes that produce short-chain fatty acids (epithelial energy source) decreases, whereas the number of microbes that produce uremic toxins increases [9].

Indoxyl sulfate and p-cresol sulfate (PCS) accumulate in the organs of patients with CKD. The local and systemic disturbances caused by the toxins in biologic metabolism and cellular signal transduction result in uremic syndrome. Chronic kidney disease perturbs inter-organ communication through small molecules, including uremic solutes and signaling molecules [10]. Moreover, IS plays a role in regulating drug-metabolizing enzymes (DMEs) and transporters during inter-organ communication [11]. In healthy individuals, the concentration of IS is 0.1–2.39 μM in healthy individuals but exceeds 500 μM in patients with advanced CKD [12]. In addition, IS is related to the progression of CVD in patients with CKD, which may be due to increased OS in the myocardium and vasculature [13]. Barreto et al. demonstrated that IS may be related to a higher CVD mortality in patients with CKD [14].

TMAO is derived from the metabolites of the gut microbiota, dietary choline, lecithin and L-carnitine. In patients with CKD, serum TMAO levels are high, which contributes to lower survival. In a mouse model, TMAO accelerated atherosclerosis by inhibiting cholesterol transfer from tissues to the liver [15]. Studies have shown that TMAO is independently related to cardiovascular events and that a relationship between TMAO levels and ischemic cardiovascular events exists, especially in CKD Stages 3b and 4 [16]. For these reasons, selective inhibition of TMAO prevents renal damage and cardiovascular events in patients with CKD [17].

4.  Effect of RSV on Traditional Cardiovascular Risk Factors

4.1.  Effect of RSV on Vascular Function

Angiotensin II (Ang II) acts on the angiotensin II type 1 receptor (AT1R) to induce the production of ROS and subsequent OS. By contrast, angiotensin 1–7 (Ang 1–7) acts on the Mas receptor (MasR) and provides protective effects. Previous studies have shown that RSV can prevent renal function deterioration, ameliorate proteinuria and improve renal histological findings in aged mice by downregulating Ang II/AT1R activity and promoting Ang 1–7/MasR activity [18]. Another study demonstrated that RSV inhibits Ang II and increases the effects of angiotensin-converting enzyme 2 (ACE2) to prevent arterial aging [19]. RSV promotes the synthesis of nitric oxide (NO) from endothelial cells and suppresses the production of endothelin-1, thereby reducing OS. Mounting evidence suggests that RSV treatment protects against the detrimental effects of induced vascular damage. Thus, RSV has protective effects on vascular function and blood pressure [20].

4.2.  Effect of RSV on Myocardial Function

Myocardial inflammation causes cardiac damage. Increased activation of NF-κB, a nuclear transcription factor responsible for the production of proinflammatory cytokines, is involved in the immune and inflammatory response of the myocardium, thereby aggravating myocardial injury [21]. In a rat model of sepsis, RSV was reported to inhibit related inflammatory factors and the NF-κB signaling pathway and activate the PI3K/mTOR signaling pathway, thereby protecting the myocardium during sepsis [22]. RSV therapy increases the expression of the autophagy biomarkers beclin-1 and LC-3II but reduces the expression of IL-6. These findings show that RSV has protective effects in ischemia-reperfusion injury in a diabetic rat model [23].

4.3.  Effect of RSV on Metabolic Syndrome Components

Metabolic syndrome increases the risk of CVD, stroke and type II diabetes. RSV acts through different mechanisms to improve the symptoms of metabolic syndrome and related disorders [24]. RSV activates SIRT-1, which activates eNOS, thereby resulting in cardioprotective, antioxidant and anti-inflammatory effects [25][26]. Tamaki et al. reported that in addition to SIRT-1, RSV activated the adenosine monophosphate-activated kinase (AMPK) signaling and Nrf2/ARE antioxidant pathways in a rat periodontitis model [27]. In addition, RSV treatment markedly reduces profibrotic protein expression and increases the expression of the ACE2/MasR axis components to increase vasodilatation and reduce blood pressure. Moreover, RSV inhibits the migration of vessel SMCs, which have important antiatherogenic and antiatherosclerotic effects [19][28].

5.  Biologic Role of RSV in Atrial Fibrillation

Atrial fibrillation (AF) and CKD usually occur together, which poses a medical dilemma because of the risk of thromboembolism and bleeding episodes [29]. RSV directly affects heart function and rhythm through cardiac remodeling and ion channel activity [30]. RSV also suppresses hypertrophic heart remodeling through the activation of SIRT-1/AMPK and the subsequent inhibition of NFAT activation, which is implicated in the evolution of AF [31], cardiac myopathy and congestive heart failure [32]. In a study investigating the therapeutic efficacy of RSV in ameliorating AF in an animal model, RSV was found to attenuate atrial fibrosis and modulate ion channels to reduce AF through the PI3K/eNOS signaling pathway [33]. Thus, the cardiovascular protective effects of RSV include reducing OS and alleviating inflammation through Nrf2 and SIRT-1 activation, upregulating the PI3K/eNOS pathway and downregulating the NF-κB pathway [34].

6.  RSV with Strong Anti-Carcinogenic Effect via Cardiovascular Protective Effects

Reactive oxygen species (ROS) play a pivotal role in the pathogenesis of both heart disease and tumor progression. Any disturbances in ROS metabolism results an increase in OS which initiates subcellular changes and resultant cardiomyopathy and heart failure. A previous study indicated that exogenous antioxidant RSV is of value in preventing both the development of heart disease and cancer by acting as ROS scavenger [35]. RSV reverses multidrug resistance in cancer cells and sensitizes cancer cells to standard chemotherapeutic agents. The proposed mechanisms of RSV to prevent carcinogenesis include the inhibition of OS, inflammation and cancer-cell proliferation and the activation of tightly regulated cell-death mechanisms [36]. RSV possesses a wide range of preventive and therapeutic options against different types of cancer [37] through its proapoptotic, antiproliferative and anti-inflammatory actions [38][39]. RSV also suppresses the malignant biologic behaviors of cancer cells, including proliferation, antiapoptosis, invasion, migration, EMT progress, levels of ROS and stemness [40]. Recently, RSV is proved be chemopreventive from tumorigenesis by targeting Sirt1 and suppression of NF-κB activation [41]. In brief, RSV provides additional anti-carcinogenic effects parallel with cardioprotective effects.

7. Conclution

The findings of this study suggest that RSV is a possible therapeutic option for patients with CKD with or without CVD. In this regard, RSV can influence the traditional and nontraditional CVD risk factors and alleviate the effects of uremic toxins in patients with CKD.

One of the nontraditional risk factors for CVD is uremic toxin-related cardiovascular side effects. IS causes electrical and structural remodeling in myocardial tissue, leading to atherosclerotic vascular disease. RSV treatment restores intestinal epithelial TJ proteins to increase epithelial integrity. RSV alters the gut microbiota to reduce indole levels in the intestinal lumen. Moreover, RSV inhibits hepatic SULT to reduce the production of uremic toxins such as IS.

In addition, RSV treatment markedly reduces the expression of pro-fibrotic proteins and increases the expression of the components of the ACE2/MasR axis to cause vasodilatation and reduce blood pressure. RSV inhibits the migration of vascular SMCs, which have important antiatherogenic and antiatherosclerotic effects [19][28]. Moreover, RSV exhibits anti-sclerotic activity in CKD by delaying disease progression. The development of RSV derivatives to reduce the occurrence of CV events in patients with CKD is warranted.

References

  1. Gansevoort, R.T.; Correa-Rotter, R.; Hemmelgarn, B.R.; Jafar, T.H.; Heerspink, H.J.L.; Mann, J.F.; Matsushita, K.; Wen, C.P. Chronic kidney disease and cardiovascular risk: Epidemiology, mechanisms, and prevention. Lancet 2013, 382, 339–352, doi:10.1016/s0140-6736(13)60595-4.
  2. Saldanha, J.F.; Leal Vde, O.; Stenvinkel, P.; Carraro-Eduardo, J.C.; Mafra, D. Resveratrol: Why is it a promising therapy for chronic kidney disease patients? Oxid. Med. Cell. Longev. 2013, 2013, 963217.
  3. Saldanha, J.F.; Leal, V.O.; Rizzetto, F.; Grimmer, G.H.; Ribeiro-Alves, M.; Daleprane, J.B.; Carraro-Eduardo, J.C.; Mafra, D. Effects of Resveratrol Supplementation in Nrf2 and NF-kappaB Expressions in Nondialyzed Chronic Kidney Disease Patients: A Randomized, Double-Blind, Placebo-Controlled, Crossover Clinical Trial. J. Ren. Nutr. 2016, 26, 401–406.
  4. Shaito, A.; Posadino, A.M.; Younes, N.; Hasan, H.; Halabi, S.; Alhababi, D.; Al-Mohannadi, A.; Abdel-Rahman, W.M.; Eid, A.; Nasrallah, G.K.; et al. Potential Adverse Effects of Resveratrol: A Literature Review. Int. J. Mol. Sci. 2020, 21, 2084, doi:10.3390/ijms21062084.
  5. Tang, W.W.; Wang, Z.; Kennedy, D.J.; Wu, Y.; Buffa, J.A.; Agatisa-Boyle, B.; Li, X.S.; Levison, B.; Hazen, S.L. Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease. Circ. Res. 2014, 116, 448–455, doi:10.1161/CIRCRESAHA.116.305360.
  6. Xia, N.; Daiber, A.; Förstermann, U.; Li, H. Antioxidant effects of resveratrol in the cardiovascular system. Br. J. Pharmacol. 2016, 174, 1633–1646, doi:10.1111/bph.13492.
  7. Ramírez-Garza, S.L.; Laveriano-Santos, E.P.L.; Marhuenda-Muñoz, M.; Storniolo, C.E.; Tresserra-Rimbau, A.; Vallverdú-Queralt, A.; Lamuela-Raventós, R.M. Health Effects of Resveratrol: Results from Human Intervention Trials. Nutr. 2018, 10, 1892, doi:10.3390/nu10121892.
  8. Vallianou, N.; Mitesh, S.; Gkogkou, A.; Geladari, E. Chronic Kidney Disease and Cardiovascular Disease: Is there Any Relationship? Curr. Cardiol. Rev. 2018, 15, 55–63, doi:10.2174/1573403x14666180711124825.
  9. Lau, W.L.; Savoj, J.; Nakata, M.B.; Vaziri, N.D. Altered microbiome in chronic kidney disease: Systemic effects of gut-derived uremic toxins. Clin. Sci. 2018, 132, 509–522, doi:10.1042/cs20171107.
  10. Caggiano, G.; Cosola, C.; Di Leo, V.; Gesualdo, M.; Gesualdo, L. Microbiome modulation to correct uremic toxins and to preserve kidney functions. Curr. Opin. Nephrol. Hypertens. 2020, 29, 49–56, doi:10.1097/mnh.0000000000000565.
  11. Nigam, S.K.; Bush, K.T. Uraemic syndrome of chronic kidney disease: Altered remote sensing and signalling. Nat. Rev. Nephrol. 2019, 15, 301–316, doi:10.1038/s41581-019-0111-1.
  12. Lekawanvijit, S.; Adrahtas, A.; Kelly, D.J.; Kompa, A.R.; Wang, B.H.; Krum, H. Does indoxyl sulfate, a uraemic toxin, have direct effects on cardiac fibroblasts and myocytes? Eur. Hear. J. 2010, 31, 1771–1779, doi:10.1093/eurheartj/ehp574.
  13. Lekawanvijit, S.; Kompa, A.R.; Wang, B.H.; Kelly, D.J.; Krum, H. Cardiorenal syndrome: The emerging role of protein-bound uremic toxins. Circ. Res. 2012, 111, 1470–1483.
  14. Barreto, F.C.; Barreto, D.V.; Liabeuf, S.; Meert, N.; Glorieux, G.; Temmar, M.; Choukroun, G.; Vanholder, R.; Massy, Z.A.; on behalf of the European Uremic Toxin Work Group (EUTox) Serum Indoxyl Sulfate Is Associated with Vascular Disease and Mortality in Chronic Kidney Disease Patients. Clin. J. Am. Soc. Nephrol. 2009, 4, 1551–1558, doi:10.2215/cjn.03980609.
  15. Koeth, R.A.; Wang, Z.; Levison, B.; Buffa, J.A.; Org, E.; Sheehy, B.T.; Britt, E.B.; Fu, X.; Wu, Y.; Li, L.; et al. Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat. Med. 2013, 19, 576–585, doi:10.1038/nm.3145.
  16. Kim, R.B.; Morse, B.L.; Djurdjev, O.; Tang, M.; Muirhead, N.; Barrett, B.; Holmes, D.T.; Madore, F.; Clase, C.M.; Rigatto, C.; et al. Advanced chronic kidney disease populations have elevated trimethylamine N-oxide levels associated with increased cardiovascular events. Kidney Int. 2016, 89, 1144–1152, doi:10.1016/j.kint.2016.01.014.
  17. Gupta, N.; Buffa, J.A.; Roberts, A.B.; Sangwan, N.; Skye, S.M.; Li, L.; Ho, K.J.; Varga, J.; DiDonato, J.A.; Tang, W.W.; et al. Targeted Inhibition of Gut Microbial Trimethylamine N-Oxide Production Reduces Renal Tubulointerstitial Fibrosis and Functional Impairment in a Murine Model of Chronic Kidney Disease. Arter. Thromb. Vasc. Boil. 2020, 40, 1239–1255, doi:10.1161/atvbaha.120.314139.
  18. Jang, I.-A.; Kim, E.N.; Lim, J.H.; Kim, M.Y.; Ban, T.H.; Yoon, H.E.; Park, C.W.; Chang, Y.S.; Choi, B.S. Effects of Resveratrol on the Renin-Angiotensin System in the Aging Kidney. Nutrient 2018, 10, 1741, doi:10.3390/nu10111741.
  19. Kim, E.N.; Kim, M.Y.; Lim, J.H.; Kim, Y.; Shin, S.J.; Park, C.W.; Kim, Y.-S.; Chang, Y.S.; Yoon, H.E.; Choi, B.S. The protective effect of resveratrol on vascular aging by modulation of the renin–angiotensin system. Atherosclerosis 2018, 270, 123–131, doi:10.1016/j.atherosclerosis.2018.01.043.
  20. Li, H.; Xia, N.; Hasselwander, S.; Daiber, A.; Li, X. Resveratrol and Vascular Function. Int. J. Mol. Sci. 2019, 20, 2155, doi:10.3390/ijms20092155.
  21. Su, Q.; Li, L.; Sun, Y.; Yang, H.; Ye, Z.; Zhao, J. Effects of the TLR4/Myd88/NF-kappaB Signaling Pathway on NLRP3 Inflammasome in Coronary Microembolization-Induced Myocardial Injury. Cell Physiol. Biochem. 2018, 47, 1497–1508.
  22. Shang, X.; Lin, K.; Yu, R.; Zhu, P.; Zhang, Y.; Wang, L.; Xu, J.; Chen, K. Resveratrol Protects the Myocardium in Sepsis by Activating the Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway and Inhibiting the Nuclear Factor-kappaB (NF-kappaB) Signaling Pathway. Med. Sci. Monit. 2019, 25, 9290–9298.
  23. Qu, X.; Chen, X.; Shi, Q.; Wang, X.; Wang, D.; Yang, L. Resveratrol alleviates ischemia/reperfusion injury of diabetic myocardium via inducing autophagy. Exp. Ther. Med. 2019, 18, 2719–2725, doi:10.3892/etm.2019.7846.
  24. Bremer, A.A. Resveratrol use in metabolic syndrome. Metab. Syndr. Relat. Disord. 2014, 12, 493–495, doi:10.1089/met.2014.1505.
  25. Bishayee, A.; Rabi, T. d-Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis. J. Carcinog. 2009, 8, 9, doi:10.4103/1477-3163.51368.
  26. Diaz-Gerevini, G.T.; Repossi, G.; Dain, A.; Tarres, M.C.; Das, U.N.; Eynard, A.R. Beneficial action of resveratrol: How and why? Nutrition 2016, 32, 174–178, doi:10.1016/j.nut.2015.08.017.
  27. Tamaki, N.; Cristina Orihuela-Campos, R.; Inagaki, Y.; Fukui, M.; Nagata, T.; Ito, H.O. Resveratrol improves oxidative stress and prevents the progression of periodontitis via the activation of the Sirt1/AMPK and the Nrf2/antioxidant defense pathways in a rat periodontitis model. Free Radic. Biol. Med. 2014, 75, 222–229.
  28. Hou, C.; Tain, Y.-L.; Yu, H.-R.; Huang, L.-T. The Effects of Resveratrol in the Treatment of Metabolic Syndrome. Int. J. Mol. Sci. 2019, 20, 535, doi:10.3390/ijms20030535.
  29. Bhatia, H.S.; Hsu, J.C.; Kim, R.J. Atrial fibrillation and chronic kidney disease: A review of options for therapeutic anticoagulation to reduce thromboembolism risk. Clin. Cardiol. 2018, 41, 1395–1402, doi:10.1002/clc.23085.
  30. Baczkó, I.; Light, P.E. Resveratrol and derivatives for the treatment of atrial fibrillation. Ann. N. Y. Acad. Sci. 2015, 1348, 68–74, doi:10.1111/nyas.12843.
  31. Lin, C.-C.; Lin, J.-L.; Lin, C.-S.; Tsai, M.-C.; Su, M.-J.; Lai, L.-P.; Huang, S.K.S. Activation of the Calcineurin-Nuclear Factor of Activated T-Cell Signal Transduction Pathway in Atrial Fibrillation. Chest 2004, 126, 1926–1932, doi:10.1016/s0012-3692(15)31443-4.
  32. Sung, M.M.; Das, S.K.; Levasseur, J.; Byrne, N.J.; Fung, D.; Kim, T.; Masson, G.; Boisvenue, J.; Soltys, C.-L.; Oudit, G.Y.; et al. Resveratrol Treatment of Mice With Pressure-Overload-Induced Heart Failure Improves Diastolic Function and Cardiac Energy Metabolism. Circ. Hear. Fail. 2014, 8, 128–137, doi:10.1161/circheartfailure.114.001677.
  33. Chong, E.; Chang, S.-L.; Hsiao, Y.-W.; Singhal, R.; Liu, S.-H.; Leha, T.; Lin, W.-Y.; Hsu, C.-P.; Chen, Y.-C.; Chen, Y.-J.; et al. Resveratrol, a red wine antioxidant, reduces atrial fibrillation susceptibility in the failing heart by PI3K/AKT/eNOS signaling pathway activation. Hear. Rhythm. 2015, 12, 1046–1056, doi:10.1016/j.hrthm.2015.01.044.
  34. Meng, X.; Zhou, J.; Zhao, C.-N.; Gan, R.-Y.; Li, H.-B. Health Benefits and Molecular Mechanisms of Resveratrol: A Narrative Review. Foods 2020, 9, 340, doi:10.3390/foods9030340.
  35. Lin, J.K.; Tsai, S.H. Chemoprevention of cancer and cardiovascular disease by resveratrol. Proc. Natl. Sci. Counc. Repub. China Part B 1999, 23, 99–106.
  36. Ko, J.-H.; Sethi, G.; Um, J.-Y.; Shanmugam, M.K.; Arfuso, F.; Kumar, A.P.; Bishayee, A.; Ahn, K.S. The Role of Resveratrol in Cancer Therapy. Int. J. Mol. Sci. 2017, 18, 2589, doi:10.3390/ijms18122589.
  37. Zhu, H.-L. Resveratrol and Its Analogues: Promising Antitumor Agents. Anti. Cancer Agents Med. Chem. 2011, 11, 479–490, doi:10.2174/187152011795677427.
  38. Shukla, Y.; Singh, R. Resveratrol and cellular mechanisms of cancer prevention. Ann. N. Y. Acad. Sci. 2011, 1215, 1–8, doi:10.1111/j.1749-6632.2010.05870.x.
  39. Rauf, A.; Imran, M.; Butt, M.S.; Nadeem, M.; Peters, D.G.; Mubarak, M.S. Resveratrol as an anti-cancer agent: A review. Crit. Rev. Food Sci. Nutr. 2017, 58, 1428–1447, doi:10.1080/10408398.2016.1263597.
  40. Jiang, Z.; Chen, K.; Cheng, L.; Yan, B.; Qian, W.; Cao, J.; Li, J.; Wu, E.; Ma, Q.; Yang, W. Resveratrol and cancer treatment: Updates. Ann. N. Y. Acad. Sci. 2017, 1403, 59–69, doi:10.1111/nyas.13466.
  41. Buhrmann, C.; Shayan, P.; Popper, B.; Goel, A.; Shakibaei, M. Sirt1 Is Required for Resveratrol-Mediated Chemopreventive Effects in Colorectal Cancer Cells. Nutrients 2016, 8, 145, doi:10.3390/nu8030145.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Pharmacology & Pharmacy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Jenn-Yeu Song
,
Ta-Chung Shen
,
Yi-Chou Hou
,
Jia-Feng Chang
,
Chien-Lin Lu
,
Wen-Chih Liu
,
Po-Jui Chen
,
Bo-Hau Chen
,
Cai-Mei Zheng
,
Kuo-Cheng Lu
View Times: 784
Revisions: 2 times (View History)
Update Date: 25 Oct 2020
Table of Contents
    1000/1000
    Hot Most Recent
    ScholarVision Creations
    Feedback