Login Register Cart 0
Generic placeholder image

Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe Translate in Chinese
Review Article

Impact of Diabetes on Cardiac and Vascular Disease: Role of Calcium Signaling

Author(s): Tarik Smani*, Isabel Gallardo-Castillo, Javier Ávila-Médina, Manuel F. Jimenez-Navarro, Antonio Ordoñez and Abdelkrim Hmadcha

Volume 26, Issue 22, 2019

Page: [4166 - 4177] Pages: 12

DOI: 10.2174/0929867324666170523140925

Price: $65

Abstract

The pathophysiology linking diabetes and cardiovascular disease (CVD) is complex and multifactorial. The specific type of cardiomyopathy associated with diabetes, known as diabetic cardiomyopathy (DCM), is recognized as asymptomatic progression of structural and functional remodeling in the heart of diabetic patients in the absence of coronary atherosclerosis and hypertension. In other words, the presence of heart disease specifically in diabetic patients is also known as diabetic heart disease. This article reviews the impact of diabetes in heart and vascular beds focusing on molecular mechanisms involving the oxidative stress, the inflammation, the endothelium dysfunction and the alteration of the homeostasis of calcium, among others mechanisms. Understanding these mechanisms will help identify and treat CVD in patients with diabetes, as well as to plan efficient strategies to mitigate DCM impact in those patients.

Keywords: Cardiovascular disease, diabetes, diabetic cardiomyopathy, calcium homeostasis, oxidative stress, endothelial dysfunction.

« Previous Next »
[1]
Diabetes Atlas, I.D.F. IDF Diabetes Atlas, 7th edn. Brussels, Belgium: International Diabetes Federation, 2015.Available at. http://www.diabetesatlas.org
[2]
Rahelić, D. [7th Edition of Idf Diabetes Atlas--Call for Immediate Action Lijec. Vjesn., 2016, 138(1-2), 57-58.
[PMID: 27290816]
[3]
Cho, N.H. Q&A: Five questions on the 2015 IDF Diabetes Atlas. Diabetes Res. Clin. Pract., 2016, 115, 157-159.
[http://dx.doi.org/10.1016/j.diabres.2016.04.048] [PMID: 27242128]
[4]
Rask-Madsen, C.; King, G.L. Vascular complications of diabetes: mechanisms of injury and protective factors. Cell Metab., 2013, 17(1), 20-33.
[http://dx.doi.org/10.1016/j.cmet.2012.11.012] [PMID: 23312281]
[5]
Hamby, R.I.; Zoneraich, S.; Sherman, L. Diabetic cardiomyopathy. JAMA, 1974, 229(13), 1749-1754.
[http://dx.doi.org/10.1001/jama.1974.03230510023016] [PMID: 4278055]
[6]
Avogaro, A.; Vigili de Kreutzenberg, S.; Negut, C.; Tiengo, A.; Scognamiglio, R. Diabetic cardiomyopathy: a metabolic perspective. Am. J. Cardiol., 2004, 93(8A), 13A-16A.
[http://dx.doi.org/10.1016/j.amjcard.2003.11.003] [PMID: 15094099]
[7]
Trost, S.U.; Belke, D.D.; Bluhm, W.F.; Meyer, M.; Swanson, E.; Dillmann, W.H. Overexpression of the sarcoplasmic reticulum Ca(2+)-ATPase improves myocardial contractility in diabetic cardiomyopathy. Diabetes, 2002, 51(4), 1166-1171.
[http://dx.doi.org/10.2337/diabetes.51.4.1166] [PMID: 11916940]
[8]
Miki, T.; Yuda, S.; Kouzu, H.; Miura, T. Diabetic cardiomyopathy: pathophysiology and clinical features. Heart Fail. Rev., 2013, 18(2), 149-166.
[http://dx.doi.org/10.1007/s10741-012-9313-3] [PMID: 22453289]
[9]
Marwick, T.H. Diabetic heart disease. Heart, 2006, 92(3), 296-300.
[PMID: 16159978]
[10]
Bers, D.M. Calcium cycling and signaling in cardiac myocytes. Annu. Rev. Physiol., 2008, 70, 23-49.
[http://dx.doi.org/10.1146/annurev.physiol.70.113006.100455] [PMID: 17988210]
[11]
Rubler, S.; Dlugash, J.; Yuceoglu, Y.Z.; Kumral, T.; Branwood, A.W.; Grishman, A. New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am. J. Cardiol., 1972, 30(6), 595-602.
[http://dx.doi.org/10.1016/0002-9149(72)90595-4] [PMID: 4263660]
[12]
Belke, D.D.; Swanson, E.A.; Dillmann, W.H. Decreased sarcoplasmic reticulum activity and contractility in diabetic db/db mouse heart. Diabetes, 2004, 53(12), 3201-3208.
[http://dx.doi.org/10.2337/diabetes.53.12.3201] [PMID: 15561951]
[13]
Ernande, L.; Derumeaux, G. Diabetic cardiomyopathy: myth or reality? Arch. Cardiovasc. Dis., 2012, 105(4), 218-225.
[http://dx.doi.org/10.1016/j.acvd.2011.11.007] [PMID: 22633296]
[14]
Pereira, L.; Matthes, J.; Schuster, I.; Valdivia, H.H.; Herzig, S.; Richard, S.; Gómez, A.M. Mechanisms of [Ca2+]i transient decrease in cardiomyopathy of db/db type 2 diabetic mice. Diabetes, 2006, 55(3), 608-615.
[http://dx.doi.org/10.2337/diabetes.55.03.06.db05-1284] [PMID: 16505222]
[15]
Hamblin, M.; Friedman, D.B.; Hill, S.; Caprioli, R.M.; Smith, H.M.; Hill, M.F. Alterations in the diabetic myocardial proteome coupled with increased myocardial oxidative stress underlies diabetic cardiomyopathy. J. Mol. Cell. Cardiol., 2007, 42(4), 884-895.
[http://dx.doi.org/10.1016/j.yjmcc.2006.12.018] [PMID: 17320100]
[16]
Nunes, S.; Soares, E.; Pereira, F.; Reis, F. The role of inflammation in diabetic cardiomyopathy. Int. J. Interferon Cytokine Mediat. Res., 2012, 4(1), 59-73.
[17]
Ding, F.; Yu, L.; Wang, M.; Xu, S.; Xia, Q.; Fu, G. O-GlcNAcylation involvement in high glucose-induced cardiac hypertrophy via ERK1/2 and cyclin D2. Amino Acids, 2013, 45(2), 339-349.
[http://dx.doi.org/10.1007/s00726-013-1504-2] [PMID: 23665912]
[18]
Kayama, Y.; Raaz, U.; Jagger, A.; Adam, M.; Schellinger, I.N.; Sakamoto, M.; Suzuki, H.; Toyama, K.; Spin, J.M.; Tsao, P.S. Diabetic cardiovascular disease induced by oxidative stress. Int. J. Mol. Sci., 2015, 16(10), 25234-25263.
[http://dx.doi.org/10.3390/ijms161025234] [PMID: 26512646]
[19]
Braunwald, E. Biomarkers in heart failure. N. Engl. J. Med., 2008, 358(20), 2148-2159.
[http://dx.doi.org/10.1056/NEJMra0800239] [PMID: 18480207]
[20]
Fernández-Velasco, M.; Ruiz-Hurtado, G.; Gómez, A.M.; Rueda, A. Ca(2+) handling alterations and vascular dysfunction in diabetes. Cell Calcium, 2014, 56(5), 397-407.
[http://dx.doi.org/10.1016/j.ceca.2014.08.007] [PMID: 25218935]
[21]
Choi, K.M.; Zhong, Y.; Hoit, B.D.; Grupp, I.L.; Hahn, H.; Dilly, K.W.; Guatimosim, S.; Lederer, W.J.; Matlib, M.A. Defective intracellular Ca(2+) signaling contributes to cardiomyopathy in Type 1 diabetic rats. Am. J. Physiol. Heart Circ. Physiol., 2002, 283(4), H1398-H1408.
[http://dx.doi.org/10.1152/ajpheart.00313.2002] [PMID: 12234790]
[22]
Peng, X.; Chen, R.; Wu, Y.; Huang, B.; Tang, C.; Chen, J.; Wang, Q.; Wu, Q.; Yang, J.; Qiu, H.; Jiang, Q. PPARγ-PI3K/AKT-NO signal pathway is involved in cardiomyocyte hypertrophy induced by high glucose and insulin. J. Diabetes Complications, 2015, 29(6), 755-760.
[http://dx.doi.org/10.1016/j.jdiacomp.2015.04.012] [PMID: 26045205]
[23]
Liu, Q.; Wang, S.; Cai, L. Diabetic cardiomyopathy and its mechanisms: Role of oxidative stress and damage. J. Diabetes Investig., 2014, 5(6), 623-634.
[http://dx.doi.org/10.1111/jdi.12250] [PMID: 25422760]
[24]
Cesselli, D.; Jakoniuk, I.; Barlucchi, L.; Beltrami, A.P.; Hintze, T.H.; Nadal-Ginard, B.; Kajstura, J.; Leri, A.; Anversa, P. Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy. Circ. Res., 2001, 89(3), 279-286.
[http://dx.doi.org/10.1161/hh1501.094115] [PMID: 11485979]
[25]
He, X.; Kan, H.; Cai, L.; Ma, Q. Nrf2 is critical in defense against high glucose-induced oxidative damage in cardiomyocytes. J. Mol. Cell. Cardiol., 2009, 46(1), 47-58.
[http://dx.doi.org/10.1016/j.yjmcc.2008.10.007] [PMID: 19007787]
[26]
Candido, R.; Forbes, J.M.; Thomas, M.C.; Thallas, V.; Dean, R.G.; Burns, W.C.; Tikellis, C.; Ritchie, R.H.; Twigg, S.M.; Cooper, M.E.; Burrell, L.M. A breaker of advanced glycation end products attenuates diabetes-induced myocardial structural changes. Circ. Res., 2003, 92(7), 785-792.
[http://dx.doi.org/10.1161/01.RES.0000065620.39919.20] [PMID: 12623881]
[27]
Bidasee, K.R.; Nallani, K.; Yu, Y.; Cocklin, R.R.; Zhang, Y.; Wang, M.; Dincer, U.D.; Besch, H.R. Jr. Chronic diabetes increases advanced glycation end products on cardiac ryanodine receptors/calcium-release channels. Diabetes, 2003, 52(7), 1825-1836.
[http://dx.doi.org/10.2337/diabetes.52.7.1825] [PMID: 12829653]
[28]
Zhao, J.; Randive, R.; Stewart, J.A. Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart. World J. Diabetes, 2014, 5(6), 860-867.
[http://dx.doi.org/10.4239/wjd.v5.i6.860] [PMID: 25512788]
[29]
Russo, I.; Frangogiannis, N.G. Diabetes-associated cardiac fibrosis: Cellular effectors, molecular mechanisms and therapeutic opportunities. J. Mol. Cell. Cardiol., 2016, 90, 84-93.
[http://dx.doi.org/10.1016/j.yjmcc.2015.12.011] [PMID: 26705059]
[30]
Battiprolu, P.K.; Lopez-Crisosto, C.; Wang, Z.V.; Nemchenko, A.; Lavandero, S.; Hill, J.A. Diabetic cardiomyopathy and metabolic remodeling of the heart. Life Sci., 2013, 92(11), 609-615.
[http://dx.doi.org/10.1016/j.lfs.2012.10.011] [PMID: 23123443]
[31]
Go, A.S.; Mozaffarian, D.; Roger, V.L.; Benjamin, E.J.; Berry, J.D.; Blaha, M.J.; Dai, S.; Ford, E.S.; Fox, C.S.; Franco, S.; Fullerton, H.J.; Gillespie, C.; Hailpern, S.M.; Heit, J.A.; Howard, V.J.; Huffman, M.D.; Judd, S.E.; Kissela, B.M.; Kittner, S.J.; Lackland, D.T.; Lichtman, J.H.; Lisabeth, L.D.; Mackey, R.H.; Magid, D.J.; Marcus, G.M.; Marelli, A.; Matchar, D.B.; McGuire, D.K.; Mohler, E.R. III; Moy, C.S.; Mussolino, M.E.; Neumar, R.W.; Nichol, G.; Pandey, D.K.; Paynter, N.P.; Reeves, M.J.; Sorlie, P.D.; Stein, J.; Towfighi, A.; Turan, T.N.; Virani, S.S.; Wong, N.D.; Woo, D.; Turner, M.B. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics--2014 update: a report from the American Heart Association. Circulation, 2014, 129(3), e28-e292.
[http://dx.doi.org/10.1161/01.cir.0000441139.02102.80] [PMID: 24352519]
[32]
Cai, L.; Kang, Y.J. Cell death and diabetic cardiomyopathy. Cardiovasc. Toxicol., 2003, 3(3), 219-228.
[http://dx.doi.org/10.1385/CT:3:3:219] [PMID: 14555788]
[33]
Cai, L.; Li, W.; Wang, G.; Guo, L.; Jiang, Y.; Kang, Y.J. Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes, 2002, 51(6), 1938-1948.
[http://dx.doi.org/10.2337/diabetes.51.6.1938] [PMID: 12031984]
[34]
Fiordaliso, F.; Li, B.; Latini, R.; Sonnenblick, E.H.; Anversa, P.; Leri, A.; Kajstura, J. Myocyte death in streptozotocin-induced diabetes in rats in angiotensin II- dependent. Lab. Invest., 2000, 80(4), 513-527.
[http://dx.doi.org/10.1038/labinvest.3780057] [PMID: 10780668]
[35]
van Hoeven, K.H.; Factor, S.M. A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease. Circulation, 1990, 82(3), 848-855.
[http://dx.doi.org/10.1161/01.CIR.82.3.848] [PMID: 2394006]
[36]
Fischer, V.W.; Barner, H.B.; Larose, L.S. Pathomorphologic aspects of muscular tissue in diabetes mellitus. Hum. Pathol., 1984, 15(12), 1127-1136.
[http://dx.doi.org/10.1016/S0046-8177(84)80307-X] [PMID: 6238897]
[37]
Tang, M.; Zhang, W.; Lin, H.; Jiang, H.; Dai, H.; Zhang, Y. High glucose promotes the production of collagen types I and III by cardiac fibroblasts through a pathway dependent on extracellular-signal-regulated kinase 1/2. Mol. Cell. Biochem., 2007, 301(1-2), 109-114.
[http://dx.doi.org/10.1007/s11010-006-9401-6] [PMID: 17206378]
[38]
van Heerebeek, L.; Hamdani, N.; Handoko, M.L.; Falcao-Pires, I.; Musters, R.J.; Kupreishvili, K.; Ijsselmuiden, A.J.; Schalkwijk, C.G.; Bronzwaer, J.G.; Diamant, M.; Borbély, A.; van der Velden, J.; Stienen, G.J.; Laarman, G.J.; Niessen, H.W.; Paulus, W.J. Diastolic stiffness of the failing diabetic heart: importance of fibrosis, advanced glycation end products, and myocyte resting tension. Circulation, 2008, 117(1), 43-51.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.107.728550] [PMID: 18071071]
[39]
Way, K.J.; Isshiki, K.; Suzuma, K.; Yokota, T.; Zvagelsky, D.; Schoen, F.J.; Sandusky, G.E.; Pechous, P.A.; Vlahos, C.J.; Wakasaki, H.; King, G.L. Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. Diabetes, 2002, 51(9), 2709-2718.
[http://dx.doi.org/10.2337/diabetes.51.9.2709] [PMID: 12196463]
[40]
Fang, Z.Y.; Prins, J.B.; Marwick, T.H. Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr. Rev., 2004, 25(4), 543-567.
[http://dx.doi.org/10.1210/er.2003-0012] [PMID: 15294881]
[41]
Zhou, G.; Li, X.; Hein, D.W.; Xiang, X.; Marshall, J.P.; Prabhu, S.D.; Cai, L. Metallothionein suppresses angiotensin II-induced nicotinamide adenine dinucleotide phosphate oxidase activation, nitrosative stress, apoptosis, and pathological remodeling in the diabetic heart. J. Am. Coll. Cardiol., 2008, 52(8), 655-666.
[http://dx.doi.org/10.1016/j.jacc.2008.05.019] [PMID: 18702970]
[42]
Brilla, C.G.; Scheer, C.; Rupp, H. Renin-angiotensin system and myocardial collagen matrix: modulation of cardiac fibroblast function by angiotensin II type 1 receptor antagonism. Journal of hypertension. Supplement : official journal of the International Society of Hypertension, 1997, 15(6), S13-19.
[http://dx.doi.org/10.1097/00004872-199715066-00004]
[43]
Kota, S.K.; Kota, S.K.; Jammula, S.; Panda, S.; Modi, K.D. Effect of diabetes on alteration of metabolism in cardiac myocytes: therapeutic implications. Diabetes Technol. Ther., 2011, 13(11), 1155-1160.
[http://dx.doi.org/10.1089/dia.2011.0120] [PMID: 21751873]
[44]
Fabiato, A. Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am. J. Physiol., 1983, 245(1), C1-C14.
[http://dx.doi.org/10.1152/ajpcell.1983.245.1.C1] [PMID: 6346892]
[45]
Bers, D.M. Cardiac excitation-contraction coupling. Nature, 2002, 415(6868), 198-205.
[http://dx.doi.org/10.1038/415198a] [PMID: 11805843]
[46]
Lee, S.L.; Ostadalova, I.; Kolar, F.; Dhalla, N.S. Alterations in Ca(2+)-channels during the development of diabetic cardiomyopathy. Mol. Cell. Biochem., 1992, 109(2), 173-179.
[PMID: 1320733]
[47]
Lu, Z.; Ballou, L.M.; Jiang, Y.P.; Cohen, I.S.; Lin, R.Z. Restoration of defective L-type Ca2+ current in cardiac myocytes of type 2 diabetic db/db mice by Akt and PKC-ι. J. Cardiovasc. Pharmacol., 2011, 58(4), 439-445.
[http://dx.doi.org/10.1097/FJC.0b013e318228e68c] [PMID: 21753738]
[48]
Shao, C.H.; Rozanski, G.J.; Patel, K.P.; Bidasee, K.R. Dyssynchronous (non-uniform) Ca2+ release in myocytes from streptozotocin-induced diabetic rats. J. Mol. Cell. Cardiol., 2007, 42(1), 234-246.
[http://dx.doi.org/10.1016/j.yjmcc.2006.08.018] [PMID: 17027851]
[49]
Yaras, N.; Ugur, M.; Ozdemir, S.; Gurdal, H.; Purali, N.; Lacampagne, A.; Vassort, G.; Turan, B. Effects of diabetes on ryanodine receptor Ca release channel (RyR2) and Ca2+ homeostasis in rat heart. Diabetes, 2005, 54(11), 3082-3088.
[http://dx.doi.org/10.2337/diabetes.54.11.3082] [PMID: 16249429]
[50]
Zhao, S.M.; Wang, Y.L.; Guo, C.Y.; Chen, J.L.; Wu, Y.Q. Progressive decay of Ca2+ homeostasis in the development of diabetic cardiomyopathy. Cardiovasc. Diabetol., 2014, 13, 75.
[http://dx.doi.org/10.1186/1475-2840-13-75] [PMID: 24712865]
[51]
Graham, S.; Gorin, Y.; Abboud, H.E.; Ding, M.; Lee, D.Y.; Shi, H.; Ding, Y.; Ma, R. Abundance of TRPC6 protein in glomerular mesangial cells is decreased by ROS and PKC in diabetes. Am. J. Physiol. Cell Physiol., 2011, 301(2), C304-C315.
[http://dx.doi.org/10.1152/ajpcell.00014.2011] [PMID: 21525431]
[52]
Wei, Z.; Wang, L.; Han, J.; Song, J.; Yao, L.; Shao, L.; Sun, Z.; Zheng, L. Decreased expression of transient receptor potential vanilloid 1 impaires the postischemic recovery of diabetic mouse hearts. Circulation journal : official journal of the Japanese Circulation Society, 2009, 73(6), 1127- 1132.
[http://dx.doi.org/10.1253/circj.CJ-08-0945]
[53]
Daskoulidou, N.; Zeng, B.; Berglund, L.M.; Jiang, H.; Chen, G.L.; Kotova, O.; Bhandari, S.; Ayoola, J.; Griffin, S.; Atkin, S.L.; Gomez, M.F.; Xu, S.Z. High glucose enhances store-operated calcium entry by upregulating ORAI/STIM via calcineurin-NFAT signalling. J. Mol. Med. (Berl.), 2015, 93(5), 511-521.
[http://dx.doi.org/10.1007/s00109-014-1234-2] [PMID: 25471481]
[54]
Freichel, M.; Schweig, U.; Stauffenberger, S.; Freise, D.; Schorb, W.; Flockerzi, V. Store-operated cation channels in the heart and cells of the cardiovascular system. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 1999, 9(4-5), 270-283.
[http://dx.doi.org/10.1159/000016321]
[55]
Eder, P.; Molkentin, J.D. TRPC channels as effectors of cardiac hypertrophy. Circ. Res., 2011, 108(2), 265-272.
[http://dx.doi.org/10.1161/CIRCRESAHA.110.225888] [PMID: 21252153]
[56]
Collins, H.E.; Zhu-Mauldin, X.; Marchase, R.B.; Chatham, J.C. STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology. Am. J. Physiol. Heart Circ. Physiol., 2013, 305(4), H446-H458.
[http://dx.doi.org/10.1152/ajpheart.00104.2013] [PMID: 23792674]
[57]
Rosado, J.A.; Diez, R.; Smani, T.; Jardín, I. STIM and orai1 variants in store-operated calcium entry. Front. Pharmacol., 2016, 6, 325.
[http://dx.doi.org/10.3389/fphar.2015.00325] [PMID: 26793113]
[58]
Domínguez-Rodríguez, A.; Ruiz-Hurtado, G.; Sabourin, J.; Gómez, A.M.; Alvarez, J.L.; Benitah, J.P. Proarrhythmic effect of sustained EPAC activation on TRPC3/4 in rat ventricular cardiomyocytes. J. Mol. Cell. Cardiol., 2015, 87, 74-78.
[http://dx.doi.org/10.1016/j.yjmcc.2015.07.002] [PMID: 26219954]
[59]
Makarewich, C.A.; Zhang, H.; Davis, J.; Correll, R.N.; Trappanese, D.M.; Hoffman, N.E.; Troupes, C.D.; Berretta, R.M.; Kubo, H.; Madesh, M.; Chen, X.; Gao, E.; Molkentin, J.D.; Houser, S.R. Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction. Circ. Res., 2014, 115(6), 567-580.
[http://dx.doi.org/10.1161/CIRCRESAHA.115.303831] [PMID: 25047165]
[60]
Gao, H.; Wang, F.; Wang, W.; Makarewich, C.A.; Zhang, H.; Kubo, H.; Berretta, R.M.; Barr, L.A.; Molkentin, J.D.; Houser, S.R. Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling. J. Mol. Cell. Cardiol., 2012, 53(5), 657-667.
[http://dx.doi.org/10.1016/j.yjmcc.2012.08.005] [PMID: 22921230]
[61]
Watanabe, H.; Murakami, M.; Ohba, T.; Takahashi, Y.; Ito, H. TRP channel and cardiovascular disease. Pharmacol. Ther., 2008, 118(3), 337-351.
[http://dx.doi.org/10.1016/j.pharmthera.2008.03.008] [PMID: 18508125]
[62]
Pang, Y.; Hunton, D.L.; Bounelis, P.; Marchase, R.B. Hyperglycemia inhibits capacitative calcium entry and hypertrophy in neonatal cardiomyocytes. Diabetes, 2002, 51(12), 3461-3467.
[http://dx.doi.org/10.2337/diabetes.51.12.3461] [PMID: 12453900]
[63]
Zhu-Mauldin, X.; Marsh, S.A.; Zou, L.; Marchase, R.B.; Chatham, J.C. Modification of STIM1 by O-linked N-acetylglucosamine (O-GlcNAc) attenuates store-operated calcium entry in neonatal cardiomyocytes. J. Biol. Chem., 2012, 287(46), 39094-39106.
[http://dx.doi.org/10.1074/jbc.M112.383778] [PMID: 22992728]
[64]
Song, J.X.; Wang, L.H.; Yao, L.; Xu, C.; Wei, Z.H.; Zheng, L.R. Impaired transient receptor potential vanilloid 1 in streptozotocin-induced diabetic hearts. Int. J. Cardiol., 2009, 134(2), 290-292.
[http://dx.doi.org/10.1016/j.ijcard.2007.12.081] [PMID: 18378339]
[65]
Sowers, J.R.; Epstein, M. Diabetes mellitus and associated hypertension, vascular disease, and nephropathy. An update. Hypertension, 1995, 26(6 Pt 1), 869-879.
[http://dx.doi.org/10.1161/01.HYP.26.6.869] [PMID: 7490142]
[66]
Calver, A.; Collier, J.; Vallance, P. Inhibition and stimulation of nitric oxide synthesis in the human forearm arterial bed of patients with insulin-dependent diabetes. J. Clin. Invest., 1992, 90(6), 2548-2554.
[http://dx.doi.org/10.1172/JCI116149] [PMID: 1469103]
[67]
Michiels, C. Endothelial cell functions. J. Cell. Physiol., 2003, 196(3), 430-443.
[http://dx.doi.org/10.1002/jcp.10333] [PMID: 12891700]
[68]
Forbes, J.M.; Cooper, M.E. Mechanisms of diabetic complications. Physiol. Rev., 2013, 93(1), 137-188.
[http://dx.doi.org/10.1152/physrev.00045.2011] [PMID: 23303908]
[69]
Potenza, M.A.; Gagliardi, S.; Nacci, C.; Carratu’, M.R.; Montagnani, M. Endothelial dysfunction in diabetes: from mechanisms to therapeutic targets. Curr. Med. Chem., 2009, 16(1), 94-112.
[http://dx.doi.org/10.2174/092986709787002853] [PMID: 19149564]
[70]
Bhargava, P.; Lee, C.H. Role and function of macrophages in the metabolic syndrome. Biochem. J., 2012, 442(2), 253-262.
[http://dx.doi.org/10.1042/BJ20111708] [PMID: 22329799]
[71]
Sasongko, M.B.; Wong, T.Y.; Jenkins, A.J.; Nguyen, T.T.; Shaw, J.E.; Wang, J.J. Circulating markers of inflammation and endothelial function, and their relationship to diabetic retinopathy. Diabet. Med., 2015, 32(5), 686-691.
[http://dx.doi.org/10.1111/dme.12640] [PMID: 25407692]
[72]
Polat, S.B.; Ugurlu, N.; Aslan, N.; Cuhaci, N.; Ersoy, R.; Cakir, B. Evaluation of biochemical and clinical markers of endothelial dysfunction and their correlation with urinary albumin excretion in patients with type 1 diabetes mellitus. Arch. Endocrinol. Metab., 2016, 60(2), 117-124.
[http://dx.doi.org/10.1590/2359-3997000000116] [PMID: 26886090]
[73]
Zeiher, A.M.; Fisslthaler, B.; Schray-Utz, B.; Busse, R. Nitric oxide modulates the expression of monocyte chemoattractant protein 1 in cultured human endothelial cells. Circ. Res., 1995, 76(6), 980-986.
[http://dx.doi.org/10.1161/01.RES.76.6.980] [PMID: 7758169]
[74]
Mohamed, A.K.; Bierhaus, A.; Schiekofer, S.; Tritschler, H.; Ziegler, R.; Nawroth, P.P. The role of oxidative stress and NF-kappaB activation in late diabetic complications. Biofactors, 1999, 10(2-3), 157-167.
[http://dx.doi.org/10.1002/biof.5520100211] [PMID: 10609877]
[75]
Cruz, N.G.; Sousa, L.P.; Sousa, M.O.; Pietrani, N.T.; Fernandes, A.P.; Gomes, K.B. The linkage between inflammation and Type 2 diabetes mellitus. Diabetes Res. Clin. Pract., 2013, 99(2), 85-92.
[http://dx.doi.org/10.1016/j.diabres.2012.09.003] [PMID: 23245808]
[76]
Ayhan, H.; Kasapkara, H.A.; Aslan, A.N.; Durmaz, T.; Keleş, T.; Akçay, M.; Akar Bayram, N.; Baştuğ, S.; Bilen, E.; Sarı, C.; Bozkurt, E. Relationship of neutrophil-to-lymphocyte ratio with aortic stiffness in type 1 diabetes mellitus. Can. J. Diabetes, 2015, 39(4), 317-321.
[http://dx.doi.org/10.1016/j.jcjd.2015.01.004] [PMID: 25797110]
[77]
Li, Y.; Ni, J.; Guo, R.; Li, W. In Patients with Coronary Artery Disease and Type 2 Diabetes, SIRT1 Expression in Circulating Mononuclear Cells Is Associated with Levels of Inflammatory Cytokines but Not with Coronary Lesions. BioMed Res. Int., 2016.20168734827
[http://dx.doi.org/10.1155/2016/8734827] [PMID: 27123454]
[78]
Tiruppathi, C.; Minshall, R.D.; Paria, B.C.; Vogel, S.M.; Malik, A.B. Role of Ca2+ signaling in the regulation of endothelial permeability. Vascul. Pharmacol., 2002, 39(4-5), 173-185.
[http://dx.doi.org/10.1016/S1537-1891(03)00007-7] [PMID: 12747958]
[79]
Yao, X.; Garland, C.J. Recent developments in vascular endothelial cell transient receptor potential channels. Circ. Res., 2005, 97(9), 853-863.
[http://dx.doi.org/10.1161/01.RES.0000187473.85419.3e] [PMID: 16254217]
[80]
Zou, M.; Dong, H.; Meng, X.; Cai, C.; Li, C.; Cai, S.; Xue, Y. Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability. PLoS One, 2015, 10(4)e0123432
[http://dx.doi.org/10.1371/journal.pone.0123432] [PMID: 25884983]
[81]
Félétou, M.; Vanhoutte, P.M. The alternative: EDHF. J. Mol. Cell. Cardiol., 1999, 31(1), 15-22.
[http://dx.doi.org/10.1006/jmcc.1998.0840] [PMID: 10072712]
[82]
Cohen, R.A.; Adachi, T. Nitric-oxide-induced vasodilatation: regulation by physiologic s-glutathiolation and pathologic oxidation of the sarcoplasmic endoplasmic reticulum calcium ATPase. Trends Cardiovasc. Med., 2006, 16(4), 109-114.
[http://dx.doi.org/10.1016/j.tcm.2006.02.001] [PMID: 16713532]
[83]
Ding, H.; Triggle, C.R. Endothelial dysfunction in diabetes: multiple targets for treatment. Pflugers Arch., 2010, 459(6), 977-994.
[http://dx.doi.org/10.1007/s00424-010-0807-3] [PMID: 20238124]
[84]
Basha, B.; Samuel, S.M.; Triggle, C.R.; Ding, H. Endothelial dysfunction in diabetes mellitus: possible involvement of endoplasmic reticulum stress? Exp. Diabetes Res., 2012.2012481840
[http://dx.doi.org/10.1155/2012/481840] [PMID: 22474423]
[85]
Shi, Y.; Vanhoutte, P.M. Reactive oxygen-derived free radicals are key to the endothelial dysfunction of diabetes. J. Diabetes, 2009, 1(3), 151-162.
[http://dx.doi.org/10.1111/j.1753-0407.2009.00030.x] [PMID: 20923534]
[86]
Mokhtar, S.S.; Vanhoutte, P.M.; Leung, S.W.; Yusof, M.I.; Wan Sulaiman, W.A.; Mat Saad, A.Z.; Suppian, R.; Rasool, A.H. Endothelium dependent hyperpolarization-type relaxation compensates for attenuated nitric oxide-mediated responses in subcutaneous arteries of diabetic patients. Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society, 2016, 53, 35-44.
[http://dx.doi.org/10.1016/j.niox.2015.12.007]
[87]
Tamareille, S.; Mignen, O.; Capiod, T.; Rücker-Martin, C.; Feuvray, D. High glucose-induced apoptosis through store-operated calcium entry and calcineurin in human umbilical vein endothelial cells. Cell Calcium, 2006, 39(1), 47-55.
[http://dx.doi.org/10.1016/j.ceca.2005.09.008] [PMID: 16243395]
[88]
Sheikh, A.Q.; Hurley, J.R.; Huang, W.; Taghian, T.; Kogan, A.; Cho, H.; Wang, Y.; Narmoneva, D.A. Diabetes alters intracellular calcium transients in cardiac endothelial cells. PLoS One, 2012, 7(5)e36840
[http://dx.doi.org/10.1371/journal.pone.0036840] [PMID: 22590623]
[89]
Bishara, N.B.; Ding, H. Glucose enhances expression of TRPC1 and calcium entry in endothelial cells. Am. J. Physiol. Heart Circ. Physiol., 2010, 298(1), H171-H178.
[http://dx.doi.org/10.1152/ajpheart.00699.2009] [PMID: 19855058]
[90]
Tiruppathi, C.; Freichel, M.; Vogel, S.M.; Paria, B.C.; Mehta, D.; Flockerzi, V.; Malik, A.B. Impairment of store-operated Ca2+ entry in TRPC4(-/-) mice interferes with increase in lung microvascular permeability. Circ. Res., 2002, 91(1), 70-76.
[http://dx.doi.org/10.1161/01.RES.0000023391.40106.A8] [PMID: 12114324]
[91]
Wang, R.; Wu, Y.; Tang, G.; Wu, L.; Hanna, S.T. Altered L-type Ca(2+) channel currents in vascular smooth muscle cells from experimental diabetic rats. Am. J. Physiol. Heart Circ. Physiol., 2000, 278(3), H714-H722.
[http://dx.doi.org/10.1152/ajpheart.2000.278.3.H714] [PMID: 10710338]
[92]
Nobe, K.; Takenouchi, Y.; Kasono, K.; Hashimoto, T.; Honda, K. Two types of overcontraction are involved in intrarenal artery dysfunction in type II diabetic mouse. J. Pharmacol. Exp. Ther., 2014, 351(1), 77-86.
[http://dx.doi.org/10.1124/jpet.114.216747] [PMID: 25085043]
[93]
Barbagallo, M.; Shan, J.; Pang, P.K.; Resnick, L.M. Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells. J. Clin. Invest., 1995, 95(2), 763-767.
[http://dx.doi.org/10.1172/JCI117724] [PMID: 7860758]
[94]
Pinho, J.F.; Medeiros, M.A.; Capettini, L.S.; Rezende, B.A.; Campos, P.P.; Andrade, S.P.; Cortes, S.F.; Cruz, J.S.; Lemos, V.S. Phosphatidylinositol 3-kinase-δ up-regulates L-type Ca2+ currents and increases vascular contractility in a mouse model of type 1 diabetes. Br. J. Pharmacol., 2010, 161(7), 1458-1471.
[http://dx.doi.org/10.1111/j.1476-5381.2010.00955.x] [PMID: 20942845]
[95]
Okon, E.B.; Szado, T.; Laher, I.; McManus, B.; van Breemen, C. Augmented contractile response of vascular smooth muscle in a diabetic mouse model. J. Vasc. Res., 2003, 40(6), 520-530.
[http://dx.doi.org/10.1159/000075238] [PMID: 14646372]
[96]
Pannirselvam, M.; Wiehler, W.B.; Anderson, T.; Triggle, C.R. Enhanced vascular reactivity of small mesenteric arteries from diabetic mice is associated with enhanced oxidative stress and cyclooxygenase products. Br. J. Pharmacol., 2005, 144(7), 953-960.
[http://dx.doi.org/10.1038/sj.bjp.0706121] [PMID: 15685205]
[97]
Navedo, M.F.; Takeda, Y.; Nieves-Cintrón, M.; Molkentin, J.D.; Santana, L.F. Elevated Ca2+ sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells. Am. J. Physiol. Cell Physiol., 2010, 298(2), C211-C220.
[http://dx.doi.org/10.1152/ajpcell.00267.2009] [PMID: 19846755]
[98]
Beech, D.J. Ion channel switching and activation in smooth-muscle cells of occlusive vascular diseases. Biochem. Soc. Trans., 2007, 35(Pt 5), 890-894.
[http://dx.doi.org/10.1042/BST0350890] [PMID: 17956239]
[99]
Chung, A.W.; Au Yeung, K.; Chum, E.; Okon, E.B.; van Breemen, C. Diabetes modulates capacitative calcium entry and expression of transient receptor potential canonical channels in human saphenous vein. Eur. J. Pharmacol., 2009, 613(1-3), 114-118.
[http://dx.doi.org/10.1016/j.ejphar.2009.04.029] [PMID: 19393642]
[100]
Mita, M.; Ito, K.; Taira, K.; Nakagawa, J.; Walsh, M.P.; Shoji, M. Attenuation of store-operated Ca2+ entry and enhanced expression of TRPC channels in caudal artery smooth muscle from Type 2 diabetic Goto-Kakizaki rats. Clin. Exp. Pharmacol. Physiol., 2010, 37(7), 670-678.
[http://dx.doi.org/10.1111/j.1440-1681.2010.05373.x] [PMID: 20337661]
[101]
Evans, J.F.; Lee, J.H.; Ragolia, L. Ang-II-induced Ca(2+) influx is mediated by the 1/4/5 subgroup of the transient receptor potential proteins in cultured aortic smooth muscle cells from diabetic Goto-Kakizaki rats. Mol. Cell. Endocrinol., 2009, 302(1), 49-57.
[http://dx.doi.org/10.1016/j.mce.2008.12.004] [PMID: 19135126]
[102]
Chaudhari, S.; Ma, R. Store-operated calcium entry and diabetic complications. Exp. Biol. Med. (Maywood), 2016, 241(4), 343-352.
[http://dx.doi.org/10.1177/1535370215609693] [PMID: 26468167]
[103]
McCormick, L.M.; Heck, P.M.; Ring, L.S.; Kydd, A.C.; Clarke, S.J.; Hoole, S.P.; Dutka, D.P. Glucagon-like peptide-1 protects against ischemic left ventricular dysfunction during hyperglycemia in patients with coronary artery disease and type 2 diabetes mellitus. Cardiovasc. Diabetol., 2015, 14, 102.
[http://dx.doi.org/10.1186/s12933-015-0259-3] [PMID: 26253538]
[104]
Díaz, I.; Smani, T. New insights into the mechanisms underlying vascular and cardiac effects of urocortin. Curr. Vasc. Pharmacol., 2013, 11(4), 457-464.
[http://dx.doi.org/10.2174/1570161111311040009] [PMID: 23905640]
[105]
Adão, R.; Santos-Ribeiro, D.; Rademaker, M.T.; Leite-Moreira, A.F.; Brás-Silva, C. Urocortin 2 in cardiovascular health and disease. Drug Discov. Today, 2015, 20(7), 906-914.
[http://dx.doi.org/10.1016/j.drudis.2015.02.012] [PMID: 25748088]
[106]
Liu, X.; Liu, C.; Li, J.; Zhang, X.; Song, F.; Xu, J. Urocortin attenuates myocardial fibrosis in diabetic rats via the Akt/GSK-3β signaling pathway. Endocr. Res., 2016, 41(2), 148-157.
[http://dx.doi.org/10.3109/07435800.2015.1094489] [PMID: 26934363]
[107]
Ruiz-Salmeron, R.; de la Cuesta-Diaz, A.; Constantino-Bermejo, M.; Pérez-Camacho, I.; Marcos-Sánchez, F.; Hmadcha, A.; Soria, B. Angiographic demonstration of neoangiogenesis after intra-arterial infusion of autologous bone marrow mononuclear cells in diabetic patients with critical limb ischemia. Cell Transplant., 2011, 20(10), 1629-1639.
[http://dx.doi.org/10.3727/096368910X0177] [PMID: 22289660]
[108]
Soria, B.; Montanya, E.; Martín, F.; Hmadcha, A. A Role for the host in the roadmap to diabetes stem cell therapy. Diabetes, 2016, 65(5), 1155-1157.
[http://dx.doi.org/10.2337/dbi16-0003] [PMID: 27208184]
[109]
Liu, M.; Chen, H.; Jiang, J.; Zhang, Z.; Wang, C.; Zhang, N.; Dong, L.; Hu, X.; Zhu, W.; Yu, H.; Wang, J. Stem cells and diabetic cardiomyopathy: from pathology to therapy. Heart Fail. Rev., 2016, 21(6), 723-736.
[http://dx.doi.org/10.1007/s10741-016-9565-4] [PMID: 27221074]
[110]
Escacena, N.; Quesada-Hernández, E.; Capilla-Gonzalez, V.; Soria, B.; Hmadcha, A. Bottlenecks in the efficient use of advanced therapy medicinal products based on mesenchymal stromal cells. Stem Cells Int., 2015, 2015895714
[http://dx.doi.org/10.1155/2015/895714] [PMID: 26273307]

Rights & Permissions Print Cite
Article Metrics
62
10
World Chagas Disease
© 2024 Bentham Science Publishers | Privacy Policy