dostęp otwarty
Ocena stężeń kotyniny oraz wybranych wskaźników odpowiedzi zapalnej u pacjentów poddawanych zabiegom endarterektomii tętnic szyjnych
dostęp otwarty
Streszczenie
Streszczenie
Słowa kluczowe
Endarterektomia, TGF-β1, nikotynizm
Tytuł
Ocena stężeń kotyniny oraz wybranych wskaźników odpowiedzi zapalnej u pacjentów poddawanych zabiegom endarterektomii tętnic szyjnych
Czasopismo
Numer
Strony
1-6
Opublikowany online
2018-07-02
Wyświetlenia strony
532
Wyświetlenia/pobrania artykułu
769
Rekord bibliograficzny
Chirurgia Polska 2017;19(1-2):1-6.
Słowa kluczowe
Endarterektomia
TGF-β1
nikotynizm
Autorzy
Elżbieta Świętochowska
Paweł Kiczmer
Alicja Prawdzic-Seńkowska
Daria Wziątek-Kuczmik
Zofia Ostrowska
Marek Motyka
- Fan J, Watanabe T. Inflammatory reactions in the pathogenesis of atherosclerosis. J Atheroscler Thromb. 2003; 10(2): 63–71.
- Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005; 352(16): 1685–1695.
- Libby P. Current Concepts of the Pathogenesis of the Acute Coronary Syndromes. Circulation. 2001; 104(3): 365–372.
- Borén J, Olin K, Lee I, et al. Identification of the principal proteoglycan-binding site in LDL. A single-point mutation in apo-B100 severely affects proteoglycan interaction without affecting LDL receptor binding. J Clin Invest. 1998; 101(12): 2658–2664.
- Libby P, Ridker PM, Maseri A, et al. Inflammation and Atherosclerosis. Circulation. 2002; 105(9): 1135–1143.
- Pentikäinen MO, Oörni K, Ala-Korpela M, et al. Modified LDL - trigger of atherosclerosis and inflammation in the arterial intima. J Intern Med. 2000; 247(3): 359–370.
- Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res. 2002; 43(9): 1363–1379.
- Li H, Horke S, Förstermann U. Vascular oxidative stress, nitric oxide and atherosclerosis. Atherosclerosis. 2014; 237(1): 208–219.
- Ishikawa Y, Kimura-Matsumoto M, Murakami M, et al. Distribution of smooth muscle cells and macrophages expressing scavenger receptor BI/II in atherosclerosis. J Atheroscler Thromb. 2009; 16(6): 829–839.
- Lewis GF, Rader DJ. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ Res. 2005; 96(12): 1221–1232.
- Hansson GK, et al. Immune and inflammatory mechanisms in the pathogenesis of atherosclerosis. Arterioscler Thromb Vasc Biol. 2001; 21(12): 1876–1890.
- Shishehbor MH, Bhatt DL. Inflammation and atherosclerosis. Curr Atheroscler Rep. 2004; 6(2): 131–139.
- Ruiz E, Redondo S, Gordillo-Moscoso A, et al. Pioglitazone induces apoptosis in human vascular smooth muscle cells from diabetic patients involving the transforming growth factor-beta/activin receptor-like kinase-4/5/7/Smad2 signaling pathway. J Pharmacol Exp Ther. 2007; 321(2): 431–438.
- Jaffe M, Sesti C, Washington IM, et al. Transforming growth factor-β signaling in myogenic cells regulates vascular morphogenesis, differentiation, and matrix synthesis. Arterioscler Thromb Vasc Biol. 2012; 32(1): e1–11.
- Feinberg MW, Watanabe M, Lebedeva MA, et al. Transforming growth factor-beta1 inhibition of vascular smooth muscle cell activation is mediated via Smad3. J Biol Chem. 2004; 279(16): 16388–16393.
- Walshe TE, Dole VS, Maharaj ASR, et al. Inhibition of VEGF or TGF-{beta} signaling activates endothelium and increases leukocyte rolling. Arterioscler Thromb Vasc Biol. 2009; 29(8): 1185–1192.
- Grainger DJ, Mosedale DE, Metcalfe JC, et al. Active and acid-activatable TGF-beta in human sera, platelets and plasma. Clin Chim Acta. 1995; 235(1): 11–31.
- Meyer A, Wang W, Qu J, et al. Platelet TGF-β1 contributions to plasma TGF-β1, cardiac fibrosis, and systolic dysfunction in a mouse model of pressure overload. Blood. 2012; 119(4): 1064–1074.
- Lutgens E, Gijbels M, Smook M, et al. Transforming growth factor-beta mediates balance between inflammation and fibrosis during plaque progression. Arterioscler Thromb Vasc Biol. 2002; 22(6): 975–982.
- Dai J, Michineau S, Franck G, et al. Long term stabilization of expanding aortic aneurysms by a short course of cyclosporine A through transforming growth factor-beta induction. PLoS One. 2011; 6(12): e28903.
- Ji Qw, Guo M, Zheng Js, et al. Downregulation of T helper cell type 3 in patients with acute coronary syndrome. Arch Med Res. 2009; 40(4): 285–293.
- Redondo S, Navarro-Dorado J, Ramajo M, et al. The complex regulation of TGF-β in cardiovascular disease. Vasc Health Risk Manag. 2012; 8: 533–539.
- Kieć-Wilk B, Stolarz-Skrzypek K, Sliwa A, et al. Peripheral blood concentrations of TGFβ1, IGF-1 and bFGF and remodelling of the left ventricle and blood vessels in hypertensive patients. Kardiol Pol. 2010; 68(9): 996–1002.
- Pallero MA, Talbert Roden M, Chen YF, et al. Stainless steel ions stimulate increased thrombospondin-1-dependent TGF-beta activation by vascular smooth muscle cells: implications for in-stent restenosis. J Vasc Res. 2010; 47(4): 309–322.
- McCaffrey TA, Du B, Fu C, et al. The expression of TGF-beta receptors in human atherosclerosis: evidence for acquired resistance to apoptosis due to receptor imbalance. J Mol Cell Cardiol. 1999; 31(9): 1627–1642.
- Sakamoto Yi, Miyazaki A, Tamagawa H, et al. Specific interaction of oxidized low-density lipoprotein with thrombospondin-1 inhibits transforming growth factor-beta from its activation. Atherosclerosis. 2005; 183(1): 85–93.
- Klebanoff SJ. Oxygen metabolism and the toxic properties of phagocytes. Ann Intern Med. 1980; 93(3): 480–489.
- Zhang R, Brennan ML, Shen Z, et al. Myeloperoxidase functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. J Biol Chem. 2002; 277(48): 46116–46122.
- Nicholls SJ, Hazen SL. Myeloperoxidase, modified lipoproteins, and atherogenesis. J Lipid Res. 2009; 50 Suppl: S346–S351.
- Hazen SL, Heinecke JW. 3-Chlorotyrosine, a specific marker of myeloperoxidase-catalyzed oxidation, is markedly elevated in low density lipoprotein isolated from human atherosclerotic intima. J Clin Invest. 1997; 99(9): 2075–2081.
- Niccoli G, Dato I, Crea F. Myeloperoxidase may help to differentiate coronary plaque erosion from plaque rupture in patients with acute coronary syndromes. Trends Cardiovasc Med. 2010; 20(8): 276–281.
- Ali M, Li Y, O'Neal WT, et al. Tobacco Exposure as Determined by Serum Cotinine and Subclinical Myocardial Injury in Individuals Free from Cardiovascular Disease. Am J Cardiol. 2017; 120(7): 1114–1117.
- Al Rifai M, DeFilippis AP, McEvoy JW, et al. The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis. 2017; 258: 119–130.
- Garbin U, Fratta Pasini A, Stranieri C, et al. Cigarette smoking blocks the protective expression of Nrf2/ARE pathway in peripheral mononuclear cells of young heavy smokers favouring inflammation. PLoS One. 2009; 4(12): e8225.
- Yamaguchi Yu, Matsuno S, Kagota S, et al. Peroxynitrite-mediated oxidative modification of low-density lipoprotein by aqueous extracts of cigarette smoke and the preventive effect of fluvastatin. Atherosclerosis. 2004; 172(2): 259–265.
- Kangavari S, Matetzky S, Shah PK, et al. Smoking increases inflammation and metalloproteinase expression in human carotid atherosclerotic plaques. J Cardiovasc Pharmacol Ther. 2004; 9(4): 291–298.
- Cavusoglu Y, Timuralp B, Us T, et al. Cigarette smoking increases plasma concentrations of vascular cell adhesion molecule-1 in patients with coronary artery disease. Angiology. 2004; 55(4): 397–402.
- Siasos G, Tsigkou V, Kokkou E, et al. Smoking and atherosclerosis: mechanisms of disease and new therapeutic approaches. Curr Med Chem. 2014; 21(34): 3936–3948.
- Messner B, Bernhard D. Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arterioscler Thromb Vasc Biol. 2014; 34(3): 509–515.
- Sirpal S. Myeloperoxidase-mediated lipoprotein carbamylation as a mechanistic pathway for atherosclerotic vascular disease. Clin Sci (Lond). 2009; 116(9): 681–695.
- Hansson GK, Libby P. The immune response in atherosclerosis: a double-edged sword. Nat Rev Immunol. 2006; 6(7): 508–519.
- Cucina A, Sapienza P, Corvino V, et al. Nicotine-induced smooth muscle cell proliferation is mediated through bFGF and TGF-beta 1. Surgery. 2000; 127(3): 316–322.
- Liu CC, Yeh HI. Nicotine: A Double-Edged Sword in Atherosclerotic Disease. Acta Cardiol Sin. 2014; 30(2): 108–113.