Antioxidant Activity and Heart Diseases
Main Article Content
Abstract
Cardiovascular disease (CVD), which are complex conditions with many pathophysiologic pathways, has increased oxidative stress as a possible common cause. For a cell to function normally, reactive oxygen species (ROS) and antioxidants must coexist in a delicate balance. High levels of ROS damage large cellular molecules including DNA, lipids and proteins, ultimately leading to necrosis and death, although their primary function is essential to shed light on biological processes. Oxidative stress, the leading cause of death globally in people with cardiovascular disease, has an impact on a variety of disorders. An increase in reactive oxygen species leads to a decrease in the availability of nitric oxide, which in turn leads to vasoconstriction and arterial hypertension. Reactive oxygen species also impair myocardial calcium processing by inducing apoptotic and hypertrophic signaling, which promote cardiac remodeling and arrhythmias. Last but not least, ROS has been shown to promote the growth of atherosclerotic plaques. This paper seeks to give an overview of oxidative stress in CVD with a focus on endothelial dysfunction before looking more closely at how it affects the most prevalent of these diseases. In order to reduce the impact of oxidative stress on CVD, appropriate nutrition and diets are reviewed afterwards.
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References
I. Tsutsui, H.; Kinugawa, S.; Matsushima, S. Oxidative stress and heart failure. Am. J. Physiol. Circ. Physiol. 2011, 301, H2181–H2190. [CrossRef] [PubMed]
II. Tahhan, A.S.; Sandesara, P.B.; Hayek, S.S.; Alkhoder, A.; Chivukula, K.; Hammadah, M.; Mohamed-Kelli, H.; O’Neal, W.T.; Topel, M.; Ghasemzadeh, N.; et al. Association between oxidative stress and atrial fibrillation. Heart Rhythm 2017, 14, 1849–1855. [CrossRef] [PubMed]
III. Baradaran, A.; Nasri, H.; Rafieian-Kopaei, M. Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants. J. Res. Med. Sci. 2014, 19, 358–367. [PubMed]
IV. Kattoor, A.J.; Pothineni, N.V.K.; Palagiri, D.; Mehta, J.L. Oxidative Stress in Atherosclerosis. Curr. Atheroscler. Rep. 2017, 19, 42. [CrossRef] [PubMed]
V. Liochev, S.I. Reactive oxygen species and the free radical theory of aging. Free Radic. Biol. Med. 2013, 60, 1–4. [CrossRef] [PubMed]
VI. Holmström, K.M.; Finkel, T. Cellular mechanisms and physiological consequences of redox-dependent signalling. Nat. Rev. Mol. Cell Biol. 2014, 15, 411–421. [CrossRef] [PubMed]
VII. Finkel, T. Signal transduction by reactive oxygen species. J. Cell Biol. 2011, 194, 7–15. [CrossRef] [PubMed]
VIII. Balaban, R.S.; Nemoto, S.; Finkel, T. Mitochondria, Oxidants, and Aging. Cell 2005, 120, 483–495. [CrossRef] [PubMed]
IX. Sies, H.; Berndt, C.; Jones, D.P. Oxidative Stress. Annu. Rev. Biochem. 2017, 86, 715–748. [CrossRef].
X. Benjamin, E.J.; Muntner, P.; Alonso, A.; Bittencourt, M.S.; Callaway, C.W.; Carson, A.P.; Chamberlain, A.M.; Chang, A.R.; Cheng, S.; Das, S.R.; et al. Heart Disease and Stroke Statistics—2019 Update: A Report from the American Heart Association. Circulation 2019, 139, 2019. [CrossRef]
XI. Huynh, D.T.N.; Heo, K.-S. Therapeutic targets for endothelial dysfunction in vascular diseases. Arch. Pharm. Res. 2019. [CrossRef] [PubMed]
XII. Volobueva, A.; Grechko, A.; Yet, S.-F.; Sobenin, I.; Orekhov, A. Changes in Mitochondrial Genome Associated with Predisposition to Atherosclerosis and Related Disease. Biomolecules 2019, 9, 377. [CrossRef] [PubMed]
XIII. Al Disi, S.S.; Anwar, M.A.; Eid, A.H. Anti-hypertensive Herbs and their Mechanisms of Action: Part I. Front. Pharmacol. 2016, 6, 323. [CrossRef] [PubMed].
XIV. Al Hariri, M.; Zibara, K.; Farhat, W.; Hashem, Y.; Soudani, N.; Al Ibrahim, F.; Hamade, E.; Zeidan, A.; Husari, A.; Kobeissy, F. Cigarette sImoking-induced cardiac hypertrophy, vascular inflammation and injury are attenuated by antioxidant supplementation in an animal model. Front. Pharmacol. 2016, 7, e397. [CrossRef].
XV. Gupta, S.C.; Hevia, D.; Patchva, S.; Park, B.; Koh, W.; Aggarwal, B.B. Upsides and downsides of reactive oxygen species for Cancer: The roles of reactive oxygen species in tumorigenesis, prevention, and therapy. Antioxid. Redox Signal 2012, 16, 1295–1322. [CrossRef].
XVI. Zorov, D.B.; Juhaszova, M.; Sollott, S.J. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. Physiol. Rev. 2014, 94, 909–950. [CrossRef] [PubMed].
XVII. Tsutsui, H.; Kinugawa, S.; Matsushima, S. Oxidative stress and heart failure. Am. J. Physiol.-Heart Circ. Physiol. 2011, 301, 2181–2190. [CrossRef] [PubMed].
XVIII. Liguori, I.; Russo, G.; Curcio, F.; Bulli, G.; Aran, L.; Della-Morte, D.; Gargiulo, G.; Testa, G.; Cacciatore, F.; Bonaduce, D.; et al. Oxidative stress, aging, and diseases. Clin. Interv. Aging 2018, 13, 757–772. [CrossRef] [PubMed].
XIX. Sharifi-Rad, M.; Kumar, N.V.A.; Zucca, P.; Varoni, E.M.; Dini, L.; Panzarini, E.; Rajkovic, J.; Fokou, P.V.T.; Azzini, E.; Peluso, I.; et al. Lifestyle, Oxidative Stress, and Antioxidants: Back and Forth in the Pathophysiology of Chronic Diseases. Front. Physiol. 2020, 11, 694. [CrossRef].
XX. Dubois-Deruy, E.; Cuvelliez, M.; Fiedler, J.; Charrier, H.; Mulder, P.; Hebbar, E.; Pfanne, A.; Beseme, O.; Chwastyniak, M.; Amouyel, P.; et al. MicroRNAs regulating superoxide dismutase 2 are new circulating biomarkers of heart failure. Sci. Rep. 2017, 7, 1–10. [CrossRef].
XXI. Strassburger, M.; Bloch, W.; Sulyok, S.; Schüller, J.; Keist, A.F.; Schmidt, A.; Wenk, J.; Peters, T.; Wlaschek, M.; Krieg, T.; et al. Heterozygous deficiency of manganese superoxide dismutase results in severe lipid peroxidation and spontaneous apoptosis in murine myocardium in vivo. Free Radic. Biol. Med. 2005, 38, 1458–1470. [CrossRef].
XXII. Li, X.; Lin, Y.; Wang, S.; Zhou, S.; Ju, J.; Wang, X.; Chen, Y.; Xia, M. Extracellular Superoxide Dismutase Is Associated With Left Ventricular Geometry and Heart Failure in Patients with Cardiovascular Disease. J. Am. Heart Assoc. 2020, 9, e016862. [CrossRef] [PubMed].
XXIII. Tehrani, H.S.; Moosavi-Movahedi, A.A. Catalase and its mysteries. Prog. Biophys. Mol. Biol. 2018, 140, 5–12. [CrossRef] [PubMed].
XXIV. Detienne, G.; De Haes, W.; Mergan, L.; Edwards, S.L.; Temmerman, L.; Van Bael, S. Beyond ROS clearance: Peroxiredoxins in stress signaling and aging. Ageing Res. Rev. 2018, 44, 33–48. [CrossRef] [PubMed].
XXV. Kuzuya, K.; Ichihara, S.; Suzuki, Y.; Inoue, C.; Ichihara, G.; Kurimoto, S.; Oikawa, S. Proteomics analysis identified peroxiredoxin 2 involved in early-phase left ventricular impairment in hamsters with cardiomyopathy. PLoS ONE 2018, 13, e0192624. [CrossRef] [PubMed].
XXVI. Ibarrola, J.; Arrieta, V.; Sádaba, R.; Martinez-Martinez, E.; Garcia-Peña, A.; Alvarez, V.; Fernández-Celis, A.; Gainza, A.; Santamaría, E.; Fernández-Irigoyen, J.; et al. Galectin-3 down-regulates antioxidant peroxiredoxin-4 in human cardiac fibroblasts: A new pathway to induce cardiac damage. Clin. Sci. 2018, 132, 1471–1485. [CrossRef].
XXVII. Cieniewski-Bernard, C.; Mulder, P.; Henry, J.-P.; Drobecq, H.; Dubois, E.; Pottiez, G.; Thuillez, C.; Amouyel, P.; Richard, V.; Pinet, F. Proteomic Analysis of Left Ventricular Remodeling in an Experimental Model of Heart Failure. J. Proteome Res. 2008, 7, 5004–5016. [CrossRef].
XXVIII. Kalyanaraman, B. Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms. Redox Biol. 2013, 1, 244–257. [CrossRef].
XXIX. Park, T.J.; Park, J.H.; Lee, G.S.; Lee, J.Y.; Shin, J.H.; Kim, M.W.; Kim, Y.S.; Kim, J.Y.; Oh, K.J.; Han, B.S.; et al. Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes. Cell Death Dis. 2019, 10, 835. [CrossRef].
XXX. Gori, T.; Münzel, T. Oxidative stress and endothelial dysfunction: Therapeutic implications. Ann. Med. 2011, 43, 259–272. [CrossRef].
XXXI. Stamler, J.S.; Osborne, J.A.; Jaraki, O.; Rabbani, L.E.; Mullins, M.; Singel, D.; Loscalzo, J. Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J. Clin. Investig. 1993, 91, 308–318. [CrossRef].
XXXII. McCully, K.S. Homocystinuria, Arteriosclerosis, Methylmalonic Aciduria, and Methyltransferase Deficiency: A Key Case Revisited. Nutr. Rev. 1992, 50, 7–12. [CrossRef].
XXXIII. Cianciolo, G.; De Pascalis, A.; Di Lullo, L.; Ronco, C.; Zannini, C.; La Manna, G. Folic acid and homocysteine in chronic kidney disease and cardiovascular disease progression: Which comes first? CardioRenal Med. 2017, 7, 255–266. [CrossRef].
XXXIV. Stroes, E.S.G.; Van Faassen, E.E.; Yo, M.; Martasek, P.; Boer, P.; Govers, R.; Rabelink, T.J. Folic acid reverts dysfunction of endothelial nitric oxide synthase. Circ. Res. 2000, 86, 1129–1134. [CrossRef] [PubMed].
XXXV. Hagar, H.H. Folic acid and vitamin B12 supplementation attenuates isoprenaline-induced myocardial infarction in experimental hyperhomocysteinemic rats. Pharmacol. Res. 2002, 46, 213–219. [CrossRef].
XXXVI. Farhangi, M.A.; Nameni, G.; Hajiluian, G.; Mesgari-Abbasi, M. Cardiac tissue oxidative stress and inflammation after vitamin D administrations in high fat- diet induced obese rats. BMC Cardiovasc. Disord. 2017, 17, 1–7. [CrossRef] [PubMed].
XXXVII. Leme Goto, P.; Cinato, M.; Merachli, F.; Vons, B.; Jimenez, T.; Marsal, D.; Todua, N.; Loi, H.; Santin, Y.; Cassel, S.; et al. In vitro and in vivo cardioprotective and metabolic efficacy of vitamin E TPGS/Apelin. J. Mol. Cell. Cardiol. 2020, 138, 165–174. [CrossRef].
XXXVIII. Wallert, M.; Ziegler, M.; Wang, X.; Maluenda, A.; Xu, X.; Yap, M.L.; Witt, R.; Giles, C.; Kluge, S.; Hortmann, M.; et al. α-Tocopherol preserves cardiac function by reducing oxidative stress and inflammation in ischemia/reperfusion injury. Redox Biol. 2019, 26, 101292. [CrossRef].
XXXIX. Banez, M.J.; Geluz, M.I.; Chandra, A.; Hamdan, T.; Biswas, O.S.; Bryan, N.S.; Von Schwarz, E.R. A systemic review on the antioxidant and anti-inflammatory effects of resveratrol, curcumin, and dietary nitric oxide supplementation on human cardiovascular health. Nutr. Res. 2020, 78, 11–26. [CrossRef].
XL. Agouni, A.; Lagrue-Lak-Hal, A.H.; Mostefai, H.A.; Tesse, A.; Mulder, P.; Rouet, P.; Desmoulin, F.; Heymes, C.; Martínez, M.C.; Andriantsitohaina, R. Red wine polyphenols prevent metabolic and cardiovascular alterations associated with obesity in Zucker fatty rats (Fa/Fa). PLoS ONE 2009, 4, e5557. [CrossRef].
XLI. Farkhondeh, T.; Folgado, S.L.; Pourbagher-Shahri, A.M.; Ashrafizadeh, M.; Samarghandian, S. The therapeutic effect of resveratrol: Focusing on the Nrf2 signaling pathway. Biomed. Pharmacother. 2020, 127, 110234. [CrossRef].
XLII. Dyck, G.J.B.; Raj, P.; Zieroth, S.; Dyck, J.R.B.; Ezekowitz, J.A. The effects of resveratrol in patients with cardiovascular disease and heart failure: A narrative review. Int. J. Mol. Sci. 2019, 20, 904. [CrossRef].
XLIII. Huang, J.P.; Hsu, S.C.; Li, D.E.; Chen, K.H.; Kuo, C.Y.; Hung, L.M. Resveratrol mitigates high-fat diet-induced vascular dysfunction by activating the Akt/eNOS/NO and Sirt1/ER pathway. J. Cardiovasc. Pharmacol. 2018, 72, 231–241. [CrossRef].
XLIV. Chan, A.Y.M.; Dolinsky, V.W.; Soltys, C.-L.M.; Viollet, B.; Baksh, S.; Light, P.E.; Dyck, J.R.B. Resveratrol inhibits cardiac hypertrophy via AMP-activated protein kinase and Akt. J. Biol. Chem. 2008, 283, 24194–24201. [CrossRef] [PubMed].
XLV. Sung, M.M.; Das, S.K.; Levasseur, J.; Byrne, N.J.; Fung, D.; Kim, T.T.; Masson, G.; Boisvenue, J.; Soltys, C.L.; Oudit, G.Y.; et al. Resveratrol treatment of mice with pressure-overloadinduced heart failure improves diastolic function and cardiac energy metabolism. Circ. Heart Fail. 2015, 8, 128–137. [CrossRef] [PubMed].
XLVI. Tanno, M.; Kuno, A.; Yano, T.; Miura, T.; Hisahara, S.; Ishikawa, S.; Shimamoto, K.; Horio, Y. Induction of manganese superoxide dismutase by nuclear translocation and activation of SIRT1 promotes cell survival in chronic heart failure. J. Biol. Chem. 2010, 285, 8375–8382. [CrossRef].
XLVII. Sabbah, H.N. Targeting mitochondrial dysfunction in the treatment of heart failure. Expert Rev. Cardiovasc. Ther. 2016, 14, 1305–1313. [CrossRef] [PubMed].
XLVIII. Senoner, T.; Dichtl, W. Oxidative stress in cardiovascular diseases: Still a therapeutic target? Nutrients 2019, 11, 2090. [CrossRef].
XLIX. Dikalova, A.E.; Bikineyeva, A.T.; Budzyn, K.; Nazarewicz, R.R.; McCann, L.; Lewis, W.; Harrison, D.G.; Dikalov, S.I. Therapeutic targeting of mitochondrial superoxide in hypertension. Circ. Res. 2010, 107, 106–116. [CrossRef].
L. Ni, R.; Cao, T.; Xiong, S.; Ma, J.; Fan, G.C.; Lacefield, J.C.; Lu, Y.; Tissier, S.L.; Peng, T. Therapeutic inhibition of mitochondrial reactive oxygen species with mito-TEMPO reduces diabetic cardiomyopathy. Free Radic. Biol. Med. 2016, 90, 12–23. [CrossRef] [PubMed].
LI. Kelso, G.F.; Porteous, C.M.; Coulter, C.V.; Hughes, G.; Porteous, W.K.; Ledgerwood, E.C.; Smith, R.A.J.; Murphy, M.P. Selective targeting of a redox-active ubiquinone to mitochondria within cells: Antioxidant and antiapoptotic properties. J. Biol. Chem. 2001, 276, 4588–4596. [CrossRef].
LII. Kim, S.; Song, J.; Ernst, P.; Latimer, M.N.; Ha, C.M.; Goh, K.Y.; Ma, W.; Rajasekaran, N.S.; Zhang, J.; Liu, X.; et al. MitoQ regulates redox-related noncoding RNAs to preserve mitochondrial network integrity in pressure-overload heart failure. Am. J. Physiol. Heart Circ. Physiol. 2020, 318, H682–H695. [CrossRef].
LIII. Rao, V.A.; Klein, S.R.; Bonar, S.J.; Zielonka, J.; Mizuno, N.; Dickey, J.S.; Keller, P.W.; Joseph, J.; Kalyanaraman, B.; Shacter, E. The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinone. J. Biol. Chem. 2010, 285, 34447–34459. [CrossRef].
LIV. Doughan, A.K.; Dikalov, S.I. Mitochondrial redox cycling of mitoquinone leads to superoxide production and cellular apoptosis. Antioxid. Redox Signal 2007, 9, 1825–1836. [CrossRef] [PubMed].
LV. Pokrzywinski, K.L.; Biel, T.G.; Kryndushkin, D.; Rao, V.A. Therapeutic targeting of the mitochondria initiates excessive superoxide production and mitochondrial depolarization causing decreased mtDNA integrity. PLoS ONE 2016, 11, e0168283. [CrossRef].
LVI. Lee, I.M.; Cook, N.R.; Gaziano, J.M.; Gordon, D.; Ridker, P.M.; Manson, J.A.E.; Hennekens, C.H.; Buring, J.E. Vitamin E in the primary prevention of cardiovascular disease and cancer. The women’s health study: A randomized controlled trial. J. Am. Med. Assoc. 2005, 294, 56–65. [CrossRef].
LVII. Toole, J.F.; Malinow, M.R.; Chambless, L.E.; Spence, J.D.; Pettigrew, L.C.; Howard, V.J.; Sides, E.G.; Wang, C.H.; Stampfer, M. Lowering Homocysteine in Patients with Ischemic Stroke to Prevent Recurrent Stroke, Myocardial Infarction, and Death: The Vitamin Intervention for Stroke Prevention (VISP) Randomized Controlled Trial. J. Am. Med. Assoc. 2004, 291, 565–575. [CrossRef].
LVIII. Lonn, E. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: A randomized controlled trial. J. Am. Med. Assoc. 2005, 293, 1338–1347.
LIX. Bønaa, K.H.; Njølstad, I.; Ueland, P.M.; Schirmer, H.; Tverdal, A.; Steigen, T.; Wang, H.; Nordrehaug, J.E.; Arnesen, E.; Rasmussen, K. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N. Engl. J. Med. 2006, 354, 1578–1588. [CrossRef].
LX. Münzel, T.; Camici, G.G.; Maack, C.; Bonetti, N.R.; Fuster, V.; Kovacic, J.C. Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series. J. Am. Coll. Cardiol. 2017, 70, 212–229. [CrossRef].
LXI. Mankowski, R.T.; You, L.; Buford, T.W.; Leeuwenburgh, C.; Manini, T.M.; Schneider, S.; Qiu, P.; Anton, S.D. Higher dose of resveratrol elevated cardiovascular disease risk biomarker levels in overweight older adults–A pilot study. Exp. Gerontol. 2020, 131, 110821. [CrossRef].
LXII. Tomé-Carneiro, J.; Gonzálvez, M.; Larrosa, M.; Yáñez-Gascón, M.J.; García-Almagro, F.J.; Ruiz-Ros, J.A.; García-Conesa, M.T.; Tomás-Barberán, F.A.; Espín, J.C. One-year consumption of a grape nutraceutical containing resveratrol improves the inflammatory and fibrinolytic status of patients in primary prevention of cardiovascular disease. Am. J. Cardiol. 2012, 110, 356–363. [CrossRef].
LXIII. Imamura, H.; Yamaguchi, T.; Nagayama, D.; Saiki, A.; Shirai, K.; Tatsuno, I. Resveratrol ameliorates arterial stiffness assessed by cardio-ankle vascular index in patients with type 2 diabetes mellitus. Int. Heart J. 2017, 58, 577–583. [CrossRef] [PubMed].
LXIV. Agarwal, B.; Campen, M.J.; Channell, M.M.; Wherry, S.J.; Varamini, B.; Davis, J.G.; Baur, J.A.; Smoliga, J.M. Resveratrol for primary prevention of atherosclerosis: Clinical trial evidence for improved gene expression in vascular endothelium. Int. J. Cardiol. 2013, 166, 246–248. [CrossRef].
LXV. Jeong, E.M.; Chung, J.; Liu, H.; Go, Y.; Gladstein, S.; Farzaneh-Far, A.; Lewandowski, E.D.; Dudley, S.C. Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction. J. Am. Heart Assoc. 2016, 5, e003046. [CrossRef] [PubMed].
LXVI. Jiménez-González, S.; Marín-Royo, G.; Jurado-López, R.; Bartolomé, M.V.; Romero-Miranda, A.; Luaces, M.; Islas, F.; Nieto, M.L.; Martínez-Martínez, E.; Cachofeiro, V. The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats. Cells 2020, 9, 451. [CrossRef].
LXVII. Van Der Made, S.M.; Plat, J.; Mensink, R.P. Resveratrol does not influence metabolic risk markers related to cardiovascular health in overweight and slightly obese subjects: A randomized, placebo-controlled crossover trial. PLoS ONE 2015, 10, e0118393. [CrossRef] [PubMed].
LXVIII. Agarwal, B.; Campen, M.J.; Channell, M.M.; Wherry, S.J.; Varamini, B.; Davis, J.G.; Baur, J.A.; Smoliga, J.M. Resveratrol for primary prevention of atherosclerosis: Clinical trial evidence for improved gene expression in vascular endothelium. Int. J. Cardiol. 2013, 166, 246–248. [CrossRef]