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CNS & Neurological Disorders - Drug Targets

Editor-in-Chief

ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

Review Article

Inhibiting Monoamine Oxidase in CNS and CVS would be a Promising Approach to Mitigating Cardiovascular Complications in Neurodegenerative Disorders

Author(s): Princika Srivastava, Sachithra Thazhathuveedu Sudevan, Arumugam Thennavan, Bijo Mathew* and S.K. Kanthlal*

Volume 23, Issue 3, 2024

Published on: 14 April, 2023

Page: [331 - 341] Pages: 11

DOI: 10.2174/1871527322666230303115236

Price: $65

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Abstract

The flavoenzyme monoamine oxidases (MAOs) are present in the mitochondrial outer membrane and are responsible for the metabolism of biogenic amines. MAO deamination of biological amines produces toxic byproducts such as amines, aldehydes, and hydrogen peroxide, which are significant in the pathophysiology of multiple neurodegenerative illnesses. In the cardiovascular system (CVS), these by-products target the mitochondria of cardiac cells leading to their dysfunction and producing redox imbalance in the endothelium of the blood vessels. This brings up the biological relationship between the susceptibility of getting cardiovascular disorders in neural patients. In the current scenario, MAO inhibitors are highly recommended by physicians worldwide for the therapy and management of various neurodegenerative disorders. Many interventional studies reveal the benefit of MAO inhibitors in CVS. Drug candidates who can target both the central and peripheral MAO could be a better to compensate for the cardiovascular comorbidities observed in neurodegenerative patients.

Keywords: Monoamine oxidases, cardiovascular system (CVS), mitochondrial outer membrane, neurodegenerative, neural patients, AD, PD.

[1]
Datta C, Bhattacharjee A. Role of Monoamine Oxidase A (MAO-A) in cardiac aging. J Cardiol Cardiovasc Sci 2020; 4(2): 31-40.
[http://dx.doi.org/10.29245/2578-3025/2020/2.1189]
[2]
Singer TP. Monoamine oxidases. Chem Biochem Flavoenzymes 1971; 2018(2): 437-70.
[3]
Kaludercic N, Carpi A, Menabò R, Di Lisa F, Paolocci N. Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury. Biochim Biophys Acta Mol Cell Res 2011; 1813(7): 1323-32.
[http://dx.doi.org/10.1016/j.bbamcr.2010.09.010] [PMID: 20869994]
[4]
Goren T, Adar L, Sasson N, Weiss YM. Clinical pharmacology tyramine challenge study to determine the selectivity of the monoamine oxidase type B (MAO-B) inhibitor rasagiline. J Clin Pharmacol 2010; 50(12): 1420-8.
[http://dx.doi.org/10.1177/0091270010369674] [PMID: 20445015]
[5]
Bieck PR, Antonin KH. Oral tyramine pressor test and the safety of monoamine oxidase inhibitor drugs: comparison of brofaromine and tranylcypromine in healthy subjects. J Clin Psychopharmacol 1988; 8(4): 237-45.
[6]
Rodríguez MJ, Saura J, Billett EE, Finch CC, Mahy N. Cellular localization of monoamine oxidase A and B in human tissues outside of the central nervous system. Cell Tissue Res 2001; 304(2): 215-20.
[http://dx.doi.org/10.1007/s004410100361] [PMID: 11396715]
[7]
Manzoor S, Hoda N. A comprehensive review of monoamine oxidase inhibitors as Anti-Alzheimer’s disease agents: A review. Eur J Med Chem 2020; 206: 112787.
[http://dx.doi.org/10.1016/j.ejmech.2020.112787] [PMID: 32942081]
[8]
Ma J, Yoshimura M, Yamashita E, Nakagawa A, Ito A, Tsukihara T. Structure of rat monoamine oxidase A and its specific recognitions for substrates and inhibitors. J Mol Biol 2004; 338(1): 103-14.
[http://dx.doi.org/10.1016/j.jmb.2004.02.032] [PMID: 15050826]
[9]
Sakai H, Tsukihara T. Structures of membrane proteins determined at atomic resolution. J Biochem 1998; 124(5): 1051-9.
[http://dx.doi.org/10.1093/oxfordjournals.jbchem.a022199] [PMID: 9832606]
[10]
Bach AW, Lan NC, Johnson DL, et al. cDNA cloning of human liver monoamine oxidase A and B: molecular basis of differences in enzymatic properties. Proc Natl Acad Sci USA 1988; 85(13): 4934-8.
[http://dx.doi.org/10.1073/pnas.85.13.4934] [PMID: 3387449]
[11]
Lu X, Rodríguez M, Gu W, Silverman RB. Inactivation of mitochondrial monoamine oxidase B by methylthio-substituted benzylamines. Bioorg Med Chem 2003; 11(20): 4423-30.
[http://dx.doi.org/10.1016/S0968-0896(03)00486-3] [PMID: 13129579]
[12]
Mathew B, Suresh J, Mathew G, Parasuraman R, Abdulla N. Plant secondary metabolites- potent inhibitors of monoamine oxidase isoforms. Cent Nerv Syst Agents Med Chem 2014; 14(1): 28-33.
[http://dx.doi.org/10.2174/1871524914666140826111930] [PMID: 25142815]
[13]
Youdim MBH, Edmondson D, Tipton KF. The therapeutic potential of monoamine oxidase inhibitors. Nat Rev Neurosci 2006; 7(4): 295-309.
[http://dx.doi.org/10.1038/nrn1883] [PMID: 16552415]
[14]
Kumar B, Sheetal S, Mantha AK, Kumar V. Recent developments on the structure-activity relationship studies of MAO inhibitors and their role in different neurological disorders. RSC Advances 2016; 6(48): 42660-83.
[http://dx.doi.org/10.1039/C6RA00302H]
[15]
Youdim MBH, Riederer P. Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition. J Neural Transm (Vienna) 1993; 91(2-3): 181-95.
[http://dx.doi.org/10.1007/BF01245231] [PMID: 8390270]
[16]
Singer TP, Ramsay RR. Monoamine oxidases: old friends hold many surprises. FASEB J 1995; 9(8): 605-10.
[http://dx.doi.org/10.1096/fasebj.9.8.7768351] [PMID: 7768351]
[17]
Schedin-Weiss S, Inoue M, Hromadkova L, et al. Monoamine oxidase B is elevated in Alzheimer disease neurons, is associated with γ-secretase and regulates neuronal amyloid β-peptide levels. Alzheimers Res Ther 2017; 9(1): 57.
[http://dx.doi.org/10.1186/s13195-017-0279-1] [PMID: 28764767]
[18]
Benedetti MS, Tipton KF. Monoamine oxidases and related amine oxidases as phase I enzymes in the metabolism of xenobiotics. J Neural Transm Suppl 1998; 52(52): 149-71.
[http://dx.doi.org/10.1007/978-3-7091-6499-0_16] [PMID: 9564617]
[19]
Reyes-Parada M, Fierro A, Iturriaga-Vasquez P, Cassels B. Monoamine Oxidase Inhibition In the Light of New Structural Data. Curr Enzym Inhib 2005; 1(1): 85-95.
[http://dx.doi.org/10.2174/1573408052952711]
[20]
Sinet PM, Heikkila RE, Cohen G. Hydrogen peroxide production by rat brain in vivo. J Neurochem 1980; 34(6): 1421-8.
[http://dx.doi.org/10.1111/j.1471-4159.1980.tb11222.x] [PMID: 7381468]
[21]
Cohen G, Kesler N. Monoamine oxidase and mitochondrial respiration. J Neurochem 1999; 73(6): 2310-5.
[http://dx.doi.org/10.1046/j.1471-4159.1999.0732310.x] [PMID: 10582588]
[22]
Saura J, Richards JG, Mahy N. Differential age-related changes of mao-a and mao-b in mouse brain and pe peripheral organs. Neurobiol Aging 1994; 15(4): 399-408.
[http://dx.doi.org/10.1016/0197-4580(94)90071-X] [PMID: 7969716]
[23]
Fowler JS, Volkow ND, Wang GJ, et al. Age-related increases in brain monoamine oxidase B in living healthy human subjects. Neurobiol Aging 1997; 18(4): 431-5.
[http://dx.doi.org/10.1016/S0197-4580(97)00037-7] [PMID: 9330975]
[24]
Erba FC. Commentary Monoamine Oxidase, Brain Ageing and Degenerative. Biochem Pharmacol 1989; 38(4): 555-61.
[http://dx.doi.org/10.1016/0006-2952(89)90198-6] [PMID: 2521790]
[25]
Saura J, Andrés N, Andrade C, Ojuel J, Eriksson K, Mahy N. Biphasic and region-specific MAO-B response to aging in normal human brain. Neurobiol Aging 1997; 18(5): 497-507.
[http://dx.doi.org/10.1016/S0197-4580(97)00113-9] [PMID: 9390776]
[26]
Tong J, Rathitharan G, Meyer JH, et al. Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders. Brain 2017; 140(9): 2460-74.
[http://dx.doi.org/10.1093/brain/awx172] [PMID: 29050386]
[27]
Nicotra A, Pierucci F, Parvez H, Senatori O. Monoamine oxidase expression during development and aging. Neurotoxicology 2004; 25(1-2): 155-65.
[http://dx.doi.org/10.1016/S0161-813X(03)00095-0] [PMID: 14697890]
[28]
O’Carroll AM, Fowler CJ, Phillips JP, Tobbia I, Tipton KF. The deamination of dopamine by human brain monoamine oxidase. Naunyn Schmiedebergs Arch Pharmacol 1983; 322(3): 198-202.
[http://dx.doi.org/10.1007/BF00500765] [PMID: 6408492]
[29]
Jones DN, Raghanti MA. The role of monoamine oxidase enzymes in the pathophysiology of neurological disorders. J Chem Neuroanat 2021; 114: 101957.
[http://dx.doi.org/10.1016/j.jchemneu.2021.101957]
[30]
Bortolato M, Shih JC. Behavioral outcomes of monoamine oxidase deficiency: Preclinical and clinical evidence. Int Rev Neurobiol 2011; 100: 13-42.
[http://dx.doi.org/10.1016/B978-0-12-386467-3.00002-9]
[31]
Tsang D, Ho KP, Wen HL. Ontogenesis of multiple forms of monoamine oxidase in rat brain regions and liver. Dev Neurosci 1986; 8(4): 243-50.
[http://dx.doi.org/10.1159/000112258] [PMID: 3829988]
[32]
Huang YH, Ito A, Arai R. Immunohistochemical localization of monoamine oxidase type B in pancreatic islets of the rat. J Histochem Cytochem 2005; 53(9): 1149-58.
[http://dx.doi.org/10.1369/jhc.5A6658.2005] [PMID: 15923360]
[33]
Huang YH, Jiang M, Fu BY. Immunocytochemical localization of monoamine oxidase type B in rat liver. Eur J Histochem 2009; 52(1): 11-8.
[http://dx.doi.org/10.4081/1181] [PMID: 18502718]
[34]
Sivasubramaniam SD, Finch CC, Rodriguez MJ, Mahy N, Billett EE. A comparative study of the expression of monoamine oxidase-A and -B mRNA and protein in non-CNS human tissues. Cell Tissue Res 2003; 313(3): 291-300.
[http://dx.doi.org/10.1007/s00441-003-0765-6] [PMID: 12898212]
[35]
Richards JG, Saura Marti J, Cesura AM, Da Prada M. Quantitative enzyme radioautography with [3H]Ro 19-6327: Localization of MAO-B in rat CNS, peripheral organs and human brain. Pharmacol Res Commun 1988; 20 (Suppl. 4): 91-2.
[http://dx.doi.org/10.1016/S0031-6989(88)80557-5]
[36]
Finberg JPM, Rabey JM. Inhibitors of MAO-A and MAO-B in psychiatry and neurology. Front Pharmacol 2016; 7(10): 340.
[http://dx.doi.org/10.3389/fphar.2016.00340] [PMID: 27803666]
[37]
Finberg JPM. Inhibitors of MAO-B and COMT: their effects on brain dopamine levels and uses in Parkinson’s disease. J Neural Transm 2019; 126(4): 433-48.
[http://dx.doi.org/10.1007/s00702-018-1952-7] [PMID: 30386930]
[38]
Kong P, Zhang B, Lei P, et al. Neuroprotection of MAO-B inhibitor and dopamine agonist in Parkinson disease. Int J Clin Exp Med 2015; 8(1): 431-9.
[PMID: 25785014]
[39]
Shioda N, Yamamoto Y, Watanabe M, Binas B, Owada Y, Fukunaga K. Heart-type fatty acid binding protein regulates dopamine D2 receptor function in mouse brain. J Neurosci 2010; 30(8): 3146-55.
[http://dx.doi.org/10.1523/JNEUROSCI.4140-09.2010] [PMID: 20181611]
[40]
Ding G, Wiegerinck RF, Shen M, Cojoc A, Zeidenweber CM, Wagner MB. Dopamine increases L-type calcium current more in newborn than adult rabbit cardiomyocytes via D1 and beta2 receptors. Am J Physiol Heart Circ Physiol 2008; 294(5): H2327-35.
[41]
Kaludercic N, Takimoto E, Nagayama T, et al. Monoamine oxidase A-mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload. Circ Res 2010; 106(1): 193-202.
[http://dx.doi.org/10.1161/CIRCRESAHA.109.198366] [PMID: 19910579]
[42]
Chidsey CA, Sonnenblick EH, Morrow AG, Braunwald E. Norepinephrine stores and contractile force of papillary muscle from the failing human heart. Circulation 1966; 33(1): 43-51.
[http://dx.doi.org/10.1161/01.CIR.33.1.43] [PMID: 5901758]
[43]
Schroeder C, Jordan J. Norepinephrine transporter function and human cardiovascular disease. Am J Physiol Heart Circ Physiol 2012; 303(11): H1273-82.
[http://dx.doi.org/10.1152/ajpheart.00492.2012]
[44]
Meltzer H. Role of serotonin in depression Ann N Y Acad Sci 1990; 600(1 The Neurophar): 486-99.
[http://dx.doi.org/ 10.1111/j.1749-6632.1990.tb16904.x] [PMID: 2252328]
[45]
Moses L. Serotonin  A review. J Vet Pharmacol Ther 2008; 31(3): 187-99.
[46]
Shimizu Y, Minatoguchi S, Hashimoto K, et al. The role of serotonin in ischemic cellular damage and the infarct size-reducing effect of sarpogrelate, a 5-hydroxytryptamine-2 receptor blocker, in rabbit hearts. J Am Coll Cardiol 2002; 40(7): 1347-55.
[http://dx.doi.org/10.1016/S0735-1097(02)02158-7] [PMID: 12383585]
[47]
Longhurst JC, Tjen-A-Looi SC, Fu LW. Cardiac sympathetic afferent activation provoked by myocardial ischemia and reperfusion. Mechanisms and reflexes. Ann N Y Acad Sci 2001; 940(1): 74-95.
[http://dx.doi.org/10.1111/j.1749-6632.2001.tb03668.x] [PMID: 11458709]
[48]
Bianchi P, Pimentel DR, Murphy MP, Colucci WS, Parini A. A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation. FASEB J 2005; 19(6): 1-15.
[http://dx.doi.org/10.1096/fj.04-2518fje] [PMID: 15703274]
[49]
Ikeda K, Tojo K, Otsubo C, et al. 5-Hydroxytryptamine synthesis in HL-1 cells and neonatal rat cardiocytes. Biochem Biophys Res Commun 2005; 328(2): 522-5.
[http://dx.doi.org/10.1016/j.bbrc.2005.01.018] [PMID: 15694378]
[50]
Rouzaud-Laborde C, Hanoun N, Baysal I, et al. Role of endothelial AADC in cardiac synthesis of serotonin and nitrates accumulation. PLoS One 2012; 7(7): e34893.
[http://dx.doi.org/10.1371/journal.pone.0034893] [PMID: 22829864]
[51]
Greene EL, Houghton O, Collinsworth G, et al. 5-HT(2A) receptors stimulate mitogen-activated protein kinase via H2O2 generation in rat renal mesangial cells. Am J Physiol Renal Physiol 2000; 278(4): F650-8.
[52]
Lee SL, Wang WW, Finlay GA, Fanburg BL. Serotonin stimulates mitogen-activated protein kinase activity through the formation of superoxide anion. Am J Physiol 1999; 277(2): L282-91.
[http://dx.doi.org/10.1152/ajplung.1999.277.2.L282]
[53]
Villeneuve C, Guilbeau-Frugier C, Sicard P, et al. p53-PGC-1α pathway mediates oxidative mitochondrial damage and cardiomyocyte necrosis induced by monoamine oxidase-A upregulation: role in chronic left ventricular dysfunction in mice. Antioxid Redox Signal 2013; 18(1): 5-18.
[http://dx.doi.org/10.1089/ars.2011.4373] [PMID: 22738191]
[54]
Behl T, Kaur D, Sehgal A, et al. Role of monoamine oxidase activity in alzheimer’s disease: An insight into the therapeutic potential of inhibitors. Molecules 2021; 26(12): 3724.
[http://dx.doi.org/10.3390/molecules26123724] [PMID: 34207264]
[55]
Emilsson L, Saetre P, Balciuniene J, Castensson A, Cairns N, Jazin EE. Increased monoamine oxidase messenger RNA expression levels in frontal cortex of Alzheimer’s disease patients. Neurosci Lett 2002; 326(1): 56-60.
[http://dx.doi.org/10.1016/S0304-3940(02)00307-5] [PMID: 12052537]
[56]
McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging‐Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 2011; 7(3): 263-9.
[http://dx.doi.org/10.1016/j.jalz.2011.03.005] [PMID: 21514250]
[57]
Carter SF, Schöll M, Almkvist O, et al. Evidence for astrocytosis in prodromal Alzheimer disease provided by 11C-deuterium-L-deprenyl: a multitracer PET paradigm combining 11C-Pittsburgh compound B and 18F-FDG. J Nucl Med 2012; 53(1): 37-46.
[http://dx.doi.org/10.2967/jnumed.110.087031] [PMID: 22213821]
[58]
Gulyás B, Pavlova E, Kása P, et al. Activated MAO-B in the brain of Alzheimer patients, demonstrated by [11C]-l-deprenyl using whole hemisphere autoradiography. Neurochem Int 2011; 58(1): 60-8.
[http://dx.doi.org/10.1016/j.neuint.2010.10.013] [PMID: 21075154]
[59]
Uddin MS, Kabir MT, Tewari D, et al. Revisiting the role of brain and peripheral Aβ in the pathogenesis of Alzheimer’s disease. J Neurol Sci 2020; 416: 116974.
[http://dx.doi.org/10.1016/j.jns.2020.116974] [PMID: 32559516]
[60]
Wingo TS, Rosen A, Cutler DJ, Lah JJ, Levey AI. Paraoxonase-1 polymorphisms in Alzheimer’s disease, Parkinson’s disease, and AD-PD spectrum diseases. Neurobiol Aging 2012; 33(1): 204.
[http://dx.doi.org/10.1016/j.neurobiolaging.2010.08.010] [PMID: 20947215]
[61]
Dluzen DE. Neuroprotective effects of estrogen upon the nigrostriatal dopaminergic system. J Neurocytol 2000; 29(5/6): 387-99.
[http://dx.doi.org/10.1023/A:1007117424491] [PMID: 11424955]
[62]
Ooi J, Hayden MR, Pouladi MA. Inhibition of excessive monoamine oxidase a/b activity protects against stress-induced neuronal death in huntington disease. Mol Neurobiol 2015; 52(3): 1850-61.
[http://dx.doi.org/10.1007/s12035-014-8974-4] [PMID: 25398695]
[63]
Ford MF, Hospital ST. Treatment of depression in Huntington’s disease with monoamine oxidase inhibitors. Br J Psychiatry 1986; 149(5): 654-6.
[http://dx.doi.org/10.1192/bjp.149.5.654] [PMID: 2949793]
[64]
Stefanovska A. Bračič M. Physics of the human cardiovascular system. Contemp Phys 1999; 40(1): 31-55.
[http://dx.doi.org/10.1080/001075199181693]
[65]
Deshwal S, Di Sante M, Di Lisa F, Kaludercic N. Emerging role of monoamine oxidase as a therapeutic target for cardiovascular disease. Curr Opin Pharmacol 2017; 33: 64-9.
[http://dx.doi.org/10.1016/j.coph.2017.04.003] [PMID: 28528298]
[66]
Inagaki T, Akiyama T, Du CK, Zhan DY, Yoshimoto M, Shirai M. Monoamine oxidase-induced hydroxyl radical production and cardiomyocyte injury during myocardial ischemia-reperfusion in rats. Free Radic Res 2016; 50(6): 645-53.
[http://dx.doi.org/10.3109/10715762.2016.1162300] [PMID: 26953687]
[67]
Truong TH, Carroll KS. Redox regulation of protein kinases. Crit Rev Biochem Mol Biol 2013; 48(4): 332-56.
[http://dx.doi.org/10.3109/10409238.2013.790873] [PMID: 23639002]
[68]
Papadopoulos CL, Kokkas BA. Oxidative stress and arterial hypertensionEp Klin Farmakol kai Farmakokinet 2002; 20(3): 117-23.
[69]
Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest 1997; 100(9): 2153-7.
[http://dx.doi.org/10.1172/JCI119751] [PMID: 9410891]
[70]
Marrero MB, Schieffer B, Paxton WG, Heerdt L, Berk BCDP. Direct stimulation of Jak/STAT pathway by the angiotensin II AT1 receptor. Nature 1995; 375(6528): 247-50.
[71]
Sundaresan M, Yu ZX, Ferrans VJ, Irani K, Finkel T. Requirement for generation of H2O2 for platelet-derived growth factor signal transduction. Science (80- ) 1995; 270(5234): 296-9.
[72]
Dubois-Deruy E, Peugnet V, Turkieh A, Pinet F. Oxidative stress in cardiovascular diseases. Antioxidants 2020; 9(9): 864.
[http://dx.doi.org/10.3390/antiox9090864] [PMID: 32937950]
[73]
Kalogeris T, Bao Y, Korthuis RJ. Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs. preconditioning. Redox Biol 2014; 2(1): 702-14.
[http://dx.doi.org/10.1016/j.redox.2014.05.006] [PMID: 24944913]
[74]
Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. Physiol Rev 2014; 94(3): 909-50.
[http://dx.doi.org/10.1152/physrev.00026.2013] [PMID: 24987008]
[75]
Skowrońska M, Zielińska M, Wójcik-Stanaszek L, et al. Ammonia increases paracellular permeability of rat brain endothelial cells by a mechanism encompassing oxidative/nitrosative stress and activation of matrix metalloproteinases. J Neurochem 2012; 121(1): 125-34.
[http://dx.doi.org/ 10.1111/j.1471-4159.2012.07669.x ] [PMID: 22260250]
[76]
Pignatelli P, De Biase L, Lenti L, et al. Tumor necrosis factor-α as trigger of platelet activation in patients with heart failure. Blood 2005; 106(6): 1992-4.
[http://dx.doi.org/10.1182/blood-2005-03-1247] [PMID: 15956282]
[77]
Davidson SM, Duchen MR. Endothelial Mitochondria. Circ Res 2007; 100(8): 1128-41.
[http://dx.doi.org/10.1161/01.RES.0000261970.18328.1d] [PMID: 17463328]
[78]
Costantini P, Chernyak BV, Petronilli V, Bernardi P. Selective inhibition of the mitochondrial permeability transition pore at the oxidation-reduction sensitive dithiol by monobromobimane. FEBS Lett 1995; 362(2): 239-42.
[http://dx.doi.org/10.1016/0014-5793(95)00256-9] [PMID: 7536690]
[79]
Chernyak BV, Bernardi P. The mitochondrial permeability transition pore is modulated by oxidative agents through both pyridine nucleotides and glutathione at two separate sites. Eur J Biochem 1996; 238(3): 623-30.
[http://dx.doi.org/10.1111/j.1432-1033.1996.0623w.x] [PMID: 8706660]
[80]
Reactive oxygen metabolites increase mitochondrial calcium in endothelial cells: implication of the Ca2+/Na+ exchanger. J Cell Sci 1999.
[81]
Zima A, Blatter L. Redox regulation of cardiac calcium channels and transporters. Cardiovasc Res 2006; 71(2): 310-21.
[http://dx.doi.org/10.1016/j.cardiores.2006.02.019] [PMID: 16581043]
[82]
Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest 1997; 100(9): 2153-7.
[83]
Kuramochi Y, Cote GM, Guo X, et al. Cardiac endothelial cells regulate reactive oxygen species-induced cardiomyocyte apoptosis through neuregulin-1β/erbB4 signaling. J Biol Chem 2004; 279(49): 51141-7.
[http://dx.doi.org/10.1074/jbc.M408662200] [PMID: 15385548]
[84]
Shah A, MacCarthy PA. Paracrine and autocrine effects of nitric oxide on myocardial function. Pharmacol Ther 2000; 86(1): 49-86.
[http://dx.doi.org/10.1016/S0163-7258(99)00072-8] [PMID: 10760546]
[85]
Bredt DS, Snyder SH. Nitric oxide, a novel neuronal messenger. Neuron 1992; 8(1): 3-11.
[http://dx.doi.org/10.1016/0896-6273(92)90104-L] [PMID: 1370373]
[86]
Napoli C, Ignarro LJ. Nitric oxide and atherosclerosis. Nitric Oxide 2001; 5(2): 88-97.
[http://dx.doi.org/10.1006/niox.2001.0337] [PMID: 11292358]
[87]
Ferdinandy P, Danial H, Ambrus I, Rothery RA, Schulz R. Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure. Circ Res 2000; 87(3): 241-7.
[http://dx.doi.org/10.1161/01.RES.87.3.241] [PMID: 10926876]
[88]
Kuhlencordt PJ, Gyurko R, Han F, et al. Accelerated atherosclerosis, aortic aneurysm formation, and ischemic heart disease in apolipoprotein E/endothelial nitric oxide synthase double-knockout mice. Circulation 2001; 104(4): 448-54.
[http://dx.doi.org/10.1161/hc2901.091399] [PMID: 11468208]
[89]
Tini G, Scagliola R, Monacelli F, et al. Alzheimer’s Disease and Cardiovascular Disease: A Particular Association. Cardiol Res Pract 2020; 2020: 1-10.
[http://dx.doi.org/10.1155/2020/2617970] [PMID: 32454996]
[90]
Surges R, Shmuely S, Dietze C, Ryvlin P, Thijs RD. Identifying patients with epilepsy at high risk of cardiac death: signs, risk factors and initial management of high risk of cardiac death. Epileptic Disord 2021; 23(1): 17-39.
[http://dx.doi.org/10.1684/epd.2021.1254] [PMID: 33650492]
[91]
Bagherieh S, Ghoshouni H, Bostan F, et al. Incidence, prevalence, and characteristics of heart failure among patients with multiple sclerosis: A systematic review and meta-analysis. Mult Scler Relat Disord 2022; 59: 103665.
[http://dx.doi.org/10.1016/j.msard.2022.103665] [PMID: 35150980]
[92]
Firoz CK, Jabir NR, Khan MS, et al. An overview on the correlation of neurological disorders with cardiovascular disease. Saudi J Biol Sci 2015; 22(1): 19-23.
[http://dx.doi.org/10.1016/j.sjbs.2014.09.003] [PMID: 25561878]
[93]
Huffman JC, Celano CM, Beach SR, Motiwala SR, Januzzi JL. Depression and cardiac disease: epidemiology, mechanisms, and diagnosis. Cardiovasc Psychiatry Neurol 2013; 2013: 1-14.
[http://dx.doi.org/10.1155/2013/695925] [PMID: 23653854]
[94]
Tahsili-Fahadan P, Geocadin RG. Heart-Brain Axis. Circ Res 2017; 120(3): 559-72.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.308446] [PMID: 28154104]
[95]
Anderson EJ, Efird JT, Davies SW, et al. Monoamine oxidase is a major determinant of redox balance in human atrial myocardium and is associated with postoperative atrial fibrillation. J Am Heart Assoc 2014; 3(1): e000713.
[http://dx.doi.org/10.1161/JAHA.113.000713] [PMID: 24572256]
[96]
Lighezan R, Sturza A, Duicu OM, et al. Monoamine oxidase inhibition improves vascular function in mammary arteries from nondiabetic and diabetic patients with coronary heart disease. Can J Physiol Pharmacol 2016; 94(10): 1040-7.
[http://dx.doi.org/10.1139/cjpp-2015-0580] [PMID: 27322151]
[97]
Griffith GC. Amine oxidase inhibitors; their current place in the therapy of cardiovascular diseases. Circulation 1960; 22(6): 1156-65.
[http://dx.doi.org/10.1161/01.CIR.22.6.1156] [PMID: 13708591]
[98]
Clinical application of the monoamine oxidase inhibitors in cardiovascular disease. Dis Nerv Syst 1960; 21(12): 1103-5.
[99]
Villeneuve C, Guilbeau-Frugier CL, Sicard P, et al. p53-PGC-1a pathway mediates oxidative mitochondrial damage and cardiomyocyte necrosis induced by monoamine oxidase-a upregulation: role in chronic left ventricular dysfunction in mice. Antioxid Redox Signal 2013; 18(1): 5-18.
[http://dx.doi.org/10.1089/ars.2011.4373] [PMID: 22738191]
[100]
Bianchi P, Kunduzova O, Masini E, et al. Oxidative stress by monoamine oxidase mediates receptor-independent cardiomyocyte apoptosis by serotonin and postischemic myocardial injury. Circulation 2005; 112(21): 3297-305.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.104.528133] [PMID: 16286591]
[101]
Flatt T. A new definition of aging? Front Genet 2012; 3: 148.
[http://dx.doi.org/10.3389/fgene.2012.00148] [PMID: 22936945]
[102]
Pchejetski D, Kunduzova O, Dayon A, et al. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res 2007; 100(1): 41-9.
[http://dx.doi.org/10.1161/01.RES.0000253900.66640.34] [PMID: 17158340]
[103]
Manni ME, Zazzeri M, Musilli C, Bigagli E, Lodovici M, Raimondi L. Exposure of cardiomyocytes to angiotensin II induces over-activation of monoamine oxidase type A: Implications in heart failure. Eur J Pharmacol 2013; 718(1-3): 271-6.
[http://dx.doi.org/10.1016/j.ejphar.2013.08.022] [PMID: 24012905]
[104]
Guglielmi P, Mathew B, Secci D, Carradori S. Chalcones: Unearthing their therapeutic possibility as monoamine oxidase B inhibitors. Eur J Med Chem 2020; 205: 112650.
[http://dx.doi.org/10.1016/j.ejmech.2020.112650] [PMID: 32920430]
[105]
Mathew B, Parambi DGT, Sivasankarapillai VS, et al. Perspective design of chalcones for the management of CNS disorders: A mini-review. CNS Neurol Disord Drug Targets 2019; 18(6): 432-45.
[http://dx.doi.org/10.2174/1871527318666190610111246] [PMID: 31187716]
[106]
Mathew B, Haridas A, Suresh J, Mathew GE, Uçar G, Jayaprakash V. Monoamine Oxidase Inhibitory Action of Chalcones: A Mini Review. Cent Nerv Syst Agents Med Chem 2016; 16(2): 120-36.
[http://dx.doi.org/10.2174/1871524915666151002124443] [PMID: 26429556]
[107]
Mathew B, Mathew GE, Petzer JP, Petzer A. Structural exploration of synthetic chromones as selective MAO-b inhibitors: a mini review. Comb Chem High Throughput Screen 2017; 20(6): 522-32.
[PMID: 28245770]
[108]
Koyiparambath VP, Prayaga Rajappan K, Rangarajan TM, et al. Deciphering the detailed structure-activity relationship of coumarins as Monoamine oxidase enzyme inhibitors-an updated review. Chem Biol Drug Des 2021; 98(4): 655-73.
[http://dx.doi.org/10.1111/cbdd.13919] [PMID: 34233082]
[109]
Bhawna KA, Kumar A, Bhatia M, Kapoor A, Kumar P, Kumar S. Monoamine oxidase inhibitors: A concise review with special emphasis on structure activity relationship studies. Eur J Med Chem 2022; 242: 114655.
[http://dx.doi.org/10.1016/j.ejmech.2022.114655] [PMID: 36037788]
[110]
Kumar S, Nair AS, Abdelgawad MA, Mathew B. Exploration of the detailed structure-activity relationships of isatin and their isomers as monoamine oxidase inhibitors. ACS Omega 2022; 7(19): 16244-59.
[http://dx.doi.org/10.1021/acsomega.2c01470] [PMID: 35601305]
[111]
Rangarajan TM, Mathew B. Recent updates on pyrazoline derivatives as promising candidates for neuropsychiatric and neurodegenerative disorders. Curr Top Med Chem 2021; 21(30): 2695-714.
[http://dx.doi.org/10.2174/1568026621999210902123132] [PMID: 34477522]
[112]
Sudevan ST, Rangarajan TM, Al-Sehemi AG, Nair AS, Koyiparambath VP, Mathew B. Revealing the role of the benzyloxy pharmacophore in the design of a new class of monoamine oxidase‐B inhibitors. Arch Pharm 2022; 355(8): 2200084.
[http://dx.doi.org/10.1002/ardp.202200084] [PMID: 35567313]
[113]
Pletscher A. The discovery of antidepressants: A winding path. Experientia 1991; 47(1): 4-8.
[http://dx.doi.org/10.1007/BF02041242] [PMID: 1999242]
[114]
Maurel A, Hernandez C, Kunduzova O, Bompart G, Cambon C, Parini A. Age-dependent increase in hydrogen peroxide production by cardiac monoamine oxidase A in rats. Am J Physiol Heart Circ Physiol 2003; 284(4): H1460-7.
[http://dx.doi.org/10.1152/ajpheart.00700.2002]

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