Quit smoking to outsmart atherogenesis: Molecular mechanisms underlying clinical evidence

Atherosclerosis

Volumn 257, Issue , 2017, Pages 242-245

  Gambardella, Jessica ^a,b   Sardu, Celestino ^c,d,e   Sacra, Cosimo ^d   Del Giudice, Carmine ^f   Santulli, Gaetano ^a,f  

^a Department of Medicine   (United States)

^b UNIVERSITY OF SALERNO   (Italy)

^c UNIVERSITY OF BERN   (Switzerland)

^d Division of Gynecologic Oncology Foundation for Research and Care John Paul II   (Italy)

^e SECOND UNIVERSITY OF NAPLES   (Italy)

^f UNIVERSITY OF NAPLES FEDERICO II   (Italy)

Author keywords

Oxidative stress; Plaque; Smoke; Smoking cessation; Thrombosis

Indexed keywords

OXIDIZING AGENT;

ANTIINFLAMMATORY ACTIVITY; ATHEROGENESIS; ATHEROSCLEROSIS; ATHEROSCLEROTIC PLAQUE; CARDIOVASCULAR RISK; EDITORIAL; HUMAN; PRIORITY JOURNAL; SMOKE; SMOKING; SMOKING CESSATION; VASCULAR REMODELING; CORONARY ARTERY DISEASE; TOBACCO USE;

ATHEROSCLEROSIS; CORONARY ARTERY DISEASE; HUMANS; SMOKING; SMOKING CESSATION; TOBACCO USE;

EID: 85009752600     PISSN: 00219150     EISSN: 18791484     Source Type: Journal    
DOI: 10.1016/j.atherosclerosis.2016.12.010     Document Type: Editorial

References (24)

1. [1] Novak, J., Olejnickova, V., Tkacova, N., et al. Mechanistic role of MicroRNAs in coupling lipid metabolism and atherosclerosis. Adv. Exp. Med. Biol. 887 (2015), 79–100.
2. [2] Ambrose, J.A., Barua, R.S., The pathophysiology of cigarette smoking and cardiovascular disease: an update. J. Am. Coll. Cardiol. 43 (2004), 1731–1737.
3. [3] Csordas, A., Bernhard, D., The biology behind the atherothrombotic effects of cigarette smoke. Nat. Rev. Cardiol. 10 (2013), 219–230.
4. [4] Lo Sasso, G., Schlage, W.K., Boue, S., et al. The Apoe(–/–) mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction. J. Transl. Med., 14, 2016, 146.
5. [5] von Holt, K., Lebrun, S., Stinn, W., et al. Progression of atherosclerosis in the Apo E–/– model: 12–month exposure to cigarette mainstream smoke combined with high–cholesterol/fat diet. Atherosclerosis 205 (2009), 135–143.
6. [6] Cheezum, M.K., et al. Association of tobacco use and cessation with coronary atherosclerosis. Atherosclerosis 257 (2017), 201–207.
7. [7] Tollefson, A.K., Oberley–Deegan, R.E., Butterfield, K.T., et al. Endogenous enzymes (NOX and ECSOD) regulate smoke–induced oxidative stress. Free Radic. Biol. Med. 49 (2010), 1937–1946.
8. [8] Rahman, M.M., Laher, I., Structural and functional alteration of blood vessels caused by cigarette smoking: an overview of molecular mechanisms. Curr. Vasc. Pharmacol. 5 (2007), 276–292.
9. [9] Boue, S., Tarasov, K., Janis, M., et al. Modulation of atherogenic lipidome by cigarette smoke in apolipoprotein E–deficient mice. Atherosclerosis 225 (2012), 328–334.
10. [10] Collins, T., Endothelial nuclear factor–kappa B and the initiation of the atherosclerotic lesion. Lab. Invest. 68 (1993), 499–508.
11. [11] Barbieri, S.S., Weksler, B.B., Tobacco smoke cooperates with interleukin–1beta to alter beta–catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase–2 expression in vitro and in vivo. FASEB J. 21 (2007), 1831–1843.
12. [12] Wang, C.N., Yang, G.H., Wang, Z.Q., et al. Role of perivascular adipose tissue in nicotineinduced endothelial cell inflammatory responses. Mol. Med. Rep. 14 (2016), 5713–5718.
13. [13] Demirjian, L., Abboud, R.T., Li, H., et al. Acute effect of cigarette smoke on TNF–alpha release by macrophages mediated through the erk1/2 pathway. Biochim. Biophys. Acta 1762 (2006), 592–597.
14. [14] Santulli, G., Wronska, A., Uryu, K., et al. A selective microRNA–based strategy inhibits restenosis while preserving endothelial function. J. Clin. Invest. 124 (2014), 4102–4114.
15. [15] Raveendran, M., Senthil, D., Utama, B., et al. Cigarette suppresses the expression of P4Halpha and vascular collagen production. Biochem. Biophys. Res. Commun. 323 (2004), 592–598.
16. [16] O'Toole, T.E., Zheng, Y.T., Hellmann, J., et al. Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages. Toxicol. Appl. Pharmacol. 236 (2009), 194–201.
17. [17] Ljungberg, L.U., Persson, K., Eriksson, A.C., et al. Effects of nicotine, its metabolites and tobacco extracts on human platelet function in vitro. Toxicol Vitro 27 (2013), 932–938.
18. [18] Kunitomo, M., Yamaguchi, Y., Kagota, S., et al. Biochemical evidence of atherosclerosis progression mediated by increased oxidative stress in apolipoprotein E–deficient spontaneously hyperlipidemic mice exposed to chronic cigarette smoke. J. Pharmacol. Sci. 110 (2009), 354–361.
19. [19] Frey, P., Waters, D.D., DeMicco, D.A., et al. Impact of smoking on cardiovascular events in patients with coronary disease receiving contemporary medical therapy (from the Treating to New Targets [TNT] and the Incremental Decrease in End Points through Aggressive Lipid Lowering [IDEAL] trials). Am. J. Cardiol. 107 (2011), 145–150.
20. [20] Lietz, M., Berges, A., Lebrun, S., et al. Cigarette–smoke–induced atherogenic lipid profiles in plasma and vascular tissue of apolipoprotein E–deficient mice are attenuated by smoking cessation. Atherosclerosis 229 (2013), 86–93.
21. [21] van Lammeren, G.W., den Ruijter, H.M., Vrijenhoek, J.E., et al. Time–dependent changes in atherosclerotic plaque composition in patients undergoing carotid surgery. Circulation 129 (2014), 2269–2276.
22. [22] Mach, L., Bedanova, H., Soucek, M., et al. Tobacco smoking and cytokine levels in human epicardial adipose tissue: Impact of smoking cessation. Atherosclerosis 255 (2016), 37–42.
23. [23] Inoue, T., Hayashi, M., Uchida, T., et al. Significance of platelet aggregability immediately after blood sampling and effect of cigarette smoking. Platelets 12 (2001), 415–418.
24. [24] Inoue-Choi, M., Liao, L.M., Reyes-Guzman, C., Hartge, P., et al. Association of Long-term, Low-Intensity Smoking With All-Cause and Cause-Specific Mortality in the National Institutes of Health-AARP Diet and Health Study. JAMA Intern. Med. 177:1 (2017), 87–95.