2020, Number 2
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CorSalud 2020; 12 (2)
N-acetylcysteine reduces myocardial injury progression in experimental models
García PA, Mora VL, Abreu RDR
Language: Spanish
References: 28
Page: 214-218
PDF size: 519.90 Kb.
ABSTRACT
N-acetylcysteine is known in a number of medical specialties and its ability to decrease the impact of reperfusion injury in acute myocardial infarction has boosted its use in cardiology over the past decades. N-acetylcysteine has a far-reaching range of effects since it functions as a protective agent against oxygen radicals through sulfhydryl groups in important regions of the cell membrane that interfere and affect endothelial functioning and complex adhesion processes as side effects; as well as other phenomena of the extravascular compartment. These processes are closely related to the cardiovascular system.
REFERENCES
Seddon M, Looi YH, Shah AM. Oxidative stress and redox signalling in cardiac hypertrophy and heart failure. Heart. 2007;93(8):903-7.
Madamanchi NR, Runge MS. Redox signaling in cardiovascular health and disease. Free Radic Biol Med. 2013;61:473-501.
Tsutsui H, Kinugawa S, Matsushima S. Oxidative stress and heart failure. Am J Physiol Heart Circ Physiol. 2011;301(6):H2181-90.
Tham YK, Bernardo BC, Ooi JY, Weeks KL, McMullen JR. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Arch Toxicol. 2015;89(9):1401-38.
Aragno M, Mastrocola R, Alloatti G, Vercellinatto I, Bardini P, Geuna S, et al. Oxidative stress triggers cardiac fibrosis in the heart of diabetic rats. Endocrinology. 2008;149(1):380-8.
Zhao W, Zhao T, Chen Y, Ahokas RA, Sun Y. Oxidative stress mediates cardiac fibrosis by enhancing transforming growth factor-beta1 in hypertensive rats. Mol Cell Biochem. 2008;317(1-2):43-50.
Worou ME, Belmokhtar K, Bonnet P, Vourc'h P, Machet MC, Khamis G, et al. Hemin decreases cardiac oxidative stress and fibrosis in a rat model of systemic hypertension via PI3K/Aktsignalling. Cardiovasc Res. 2011;91(2):320-9.
Li YQ, Li XB, Guo SJ, Chu SL, Gao PJ, Zhu DL, et al. Apocynin attenuates oxidative stress and cardiac fibrosis in angiotensin II-induced cardiac diastolic dysfunction in mice. Acta Pharmacol Sin. 2013;34(3):352-9.
Talasaz AH, Khalili H, Jenab Y, Salarifar M, Broumand MA, Darabi F. N-Acetylcysteine effects on transforming growth factor-ß and tumor necrosis factor-a serum levels as pro-fibrotic and inflammatory biomarkers in patients following ST-segment elevation myocardial infarction. Drugs R D. 2013;13(3):199-205.
Lehrer SS, Geeves MA. The myosin-activated thin filament regulatory state, M?-open: a link to hypertrophic cardiomyopathy (HCM). J Muscle Res Cell Motil. 2014;35(2):153-60.
Cazzola M, Calzetta L, Page C, Jardim J, Chuchalin AG, Rogliani P, et al. Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a meta-analysis. Eur Respir Rev. 2015;24(137):451-61.
Lasram MM, Lamine AJ, Dhouib IB, Bouzid K, Annabi A, Belhadjhmida N, et al. Antioxidant and anti-inflammatory effects of N-acetylcysteine against malathion-induced liver damages and immunotoxicity in rats. Life Sci. 2014;107(1-2):50-8.
Drazner MH. The progression of hypertensive heart disease. Circulation. 2011;123(3):327-34.
Crozatier B, Ventura-Clapier R. Inhibition of hypertrophy, per se, may not be a good therapeutic strategy in ventricular pressure overload: other approaches could be more beneficial. Circulation. 2015;131(16):1448-57.
Zwadlo C, Schmidtmann E, Szaroszyk M, Kattih B, Froese N, Hinz H, et al. Antiandrogenic therapy with finasteride attenuates cardiac hypertrophy and left ventricular dysfunction. Circulation. 2015;131(12):1071-81.
Sag CM, Santos CX, Shah AM. Redox regulation of cardiac hypertrophy. J Mol Cell Cardiol. 2014;73:103-11.
Münzel T, Gori T, Keaney JF, Maack C, Daiber A. Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications. Eur Heart J. 2015;36(38):2555-64.
Altenhöfer S, Radermacher KA, Kleikers PW, Wingler K, Schmidt HH. Evolution of NADPH oxidase inhibitors: Selectivity and mechanisms for target engagement. Antioxid Redox Signal. 2015;23(5):406-27.
Fratelli M, Goodwin LO, Ørom UA, Lombardi S, Tonelli R, Mengozzi M, et al. Gene expression profiling reveals a signaling role of glutathione in redox regulation. Proc Natl Acad Sci U S A. 2005;102(39):13998-4003.
Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacol Ther. 2014;141(2):150-9.
Adamy C, Mulder P, Khouzami L, Andrieu-abadie N, Defer N, Candiani G, et al. Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats. J Mol Cell Cardiol. 2007;43(3):344-53.
Lombardi R, Rodriguez G, Chen SN, Ripplinger CM, Li W, Chen J, et al. Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms. Circulation. 2009;119(10):1398-407.
Foltz WU, Wagner M, Rudakova E, Volk T. N-acetylcysteine prevents electrical remodeling and attenuates cellular hypertrophy in epicardial myocytes of rats with ascending aortic stenosis. Basic Res Cardiol [Internet]. 2012 [citado 11/02/2019];107(5):290. Disponible en: http://doi. org/10. 1007/s00395-012-0290-4
Reyes DR, Gomes MJ, Rosa CM, Pagan LU, Damatto FC, Damatto RL, et al. N-Acetylcysteine influence on oxidative stress and cardiac remodeling in rats during transition from compensated left ventricular hypertrophy to heart failure. Cell Physiol Biochem. 2017;44(6):2310-21.
Giam B, Chu PY, Kuruppu S, Smith AI, Horlock D, Kiriazis H, et al. N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure. Physiol Rep [Internet]. 2016 [citado 12/02/2020];4(7):e12757. Disponible en: http://doi. org/10. 14814/phy2. 12757
Tsai CT, Wu CK, Lee JK, Chang SN, Kuo YM, Wang YC, et al. TNF-a down-regulates sarcoplasmic reticulum Ca²? ATPase expression and leads to left ventricular diastolic dysfunction through binding of NF-?B to promoter response element. Cardiovasc Res. 2015;105(3):318-29.
Alves ML, Dias FA, Gaffin RD, Simon JN, Montminy EM, Biesiadecki BJ, et al. Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filamento proteins. Circ Cardiovasc Genet. 2014;7(2):132-43.
Wilder T, Ryba DM, Wieczorek DF, Wolska BM, Solaro RJ. N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy. Am J Physiol Heart Circ Physiol. 2015;309(10):H1720-30.