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Adriyamisinin Neden olduğu Kalp Yetmezliğinde HMGB-1 ve AMPK’nin Olası Etkileri

Yıl 2015, Cilt: 1 Sayı: 1, 29 - 33, 15.04.2015

Öz

Adriyamisin (ADR), kanser tedavisinde yaygın olarak kullanılan
antikanser bir ilaçtır. ADR kalp, karaciğer, böbrek, testis gibi
birçok dokuda toksik etkiye sebep olur. Fakat en çok kalp
dokusunda bu toksik etkisi ortaya çıkar. ADR’ nin kalp
yetmezliğine yol açan mekanizma/mekanizmaları hala tam olarak
aydınlatılamamıştır. Bundan dolayı kalp yetmezliğine yönelik
etkin bir tedavi de hala geliştirilememiştir. Günümüze kadar
yapılmış çalışmalarda en yaygın görüş, bu toksik etkiye reaktif
oksijen türleri’nin (ROS) aracılık ettiğidir. HMGB1 (High
Mobility Group Box 1), türler arasında oldukça iyi korunmuş bir
kromatin proteindir. HMGB1, çekirdekte transkripsiyon faktörleri,
DNA’nın histon proteinleri ile ilişkilidir. HMGB1 DNA’yı
organize eder ve transkripsiyonu düzenler. Bu protein hücrenin
sağ kalım ve ölüm yolakları ile ilişkilidir. Yapılan çalışmalarda,
HMGB1’nin sadece stres durumlarında değil, aynı zamanda
patolojik koşullarda da salgılandığı gösterilmiştir. HMGB1
apoptozisi uyarır. ADR, mitokondride üretilen enerji miktarının
azalmasına neden olur. Normal koşullarda, hücrede tüketilen ATP
neticesinde AMP/ATP oranı artmaktadır. Bu artış AMP-aktive
edilmiş kinaz (AMPK) aracılığıyla hücrede depolanan ATP’nin
kullanılmasını sağlar. ADR’nin neden olduğu enerji stresinin
AMPK sistemini aktive etmesi beklenir. Fakat ilginç bir şekilde
ADR’nin AMPK’ı baskıladığı gösterilmiştir. Mitokondriyal enerji
üretiminin azalmasına ek olarak AMPK sisteminin baskılanması
kalp kası hücrelerinde enerji açığının artmasına ve apoptozis
sürecinin hızlanmasına katkı sağlıyor olabilir. AMPK de hücre
sağ kalım ve ölüm sistemleri ile yakından ilişkili bir proteindir.
AMPK’nin, baskılandığında apoptozisi çeşitli yollardan (KAS,
p53 vb) aktive ettiği bulunmuştur. ROS’un ADR’nin
kardiyotoksisitesine aracılık ettiği kanısından dolayı da tedavi için
antioksidan maddeler kullanıldı ve sadece kalp yetmezliğinin
hafifletilebildiği bildirilmektedir. Dolayısıyla, ADR’nin kalp
yetmezliğini başlatan sinyal molekülünü bulmaya odaklanmak bu
sorunun çözümünü sağlayabilir.

Kaynakça

  • Wilking N, Jönsson B, Högberg D. "Patient Access to Cancer Drugs http://www.comparatorreports.se/Patient%20Access%20to%2 0Cancer%20Treatment%20in%20Turkey.pdf. Son erişim tarihi: 14 Şubat 2014. Turkey"
  • Minami M, Matsumoto S, Horiuchi H. Cardiovascular side- effects of modern cancer therapy. Circ J 2010; 74, 1779-86.
  • Horacek JM, Vasatova M, Pudil R, Tichy M, Zak P, Jakl M, Jebavy L, Maly J. Biomarkers for the early detection of anthracycline-induced cardiotoxicity: current status. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014; 158 (4): 511-517.
  • Jemal A, Siegel R, Ward E, Murray T, Xu J. Smigal C, Thun M.J. Cancer statistics. CA Cancer J Clin 2006; 56(2):106-30.
  • Bristow MR, Thompson PD, Martin RP, Mason JW, Billingham cardiotoxicity. Am J Med 1978; 65(5): 823-32. Early anthracycline
  • Bleyer WA. The impact of childhood cancer on the United States and the world. CA Cancer J Clin 1990; 40(6): 355-67.
  • Johnson BA, Cheang MS, Goldenberg GJ. Comparison of adriamycin uptake in chick embryo heart and liver cells an murine L5178Y lymphoblasts in vitro: role of drug uptake in cardiotoxicity. Cancer Res1986; 46(1): 218-23.
  • Huber SA. Doxorubicin-induced alterations in cultured myocardial cells stimulate cytolytic T lymphocyte responses. Am J Pathol 1990; 137(2): 449-56.
  • Doroshow JH, Locker GY, Myers CE. Enzymatic defenses of the mouse heart against reactive oxygen metabolites: alterations produced by doxorubicin. J Clin Invest 1980; 65(1): 128-35.
  • Berthiaume JM, Wallace KB. Adriamycin-induced oxidative mitochondrial cardiotoxicity. Cell Biol Toxicol 2007; 23(1): 15- 25.
  • Tokarska-Schlattner M, Zaugg M, Zuppinger C, Wallimann T, Schlattner U. New insights into doxorubicin-induced cardiotoxicity: the critical role of cellular energetics. J Mol Cell Cardiol 2006; 41(3): 389-405.
  • Goormaghtigh E, Huart P, Praet M, Brasseur R, Ruysschaert JM. Structure of the adriamycin-cardiolipin complex. Role in mitochondrial toxicity. Biophys Chem 1990; 35(2): 247-57.
  • Monteiro JP, Oliveira PJ, Jurado AS. Mitochondrial membrane lipid remodeling in pathophysiology: a new target for diet and therapeutic interventions. Prog Lipid Res 2013; 52(4): 513-28.
  • Simunek T, Sterba M, Popelova O, Adamcova M, Hrdina R, Gersl, V. Anthracycline-induced cardiotoxicity: overview of studies examining the roles of oxidative stress and free cellular iron. Pharmacol Rep 2009; 61(1): 154-71.
  • Minotti G, Menna P, Salvatorelli E, Cairo G, Gianni L. Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity. Pharmacol Rev 2004; 56(2): 185-229.
  • Kubasiak LA, Hernandez OM, Bishopric NH, Webster KA. Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3. Proc Natl Acad Sci U S A 2002; 99(20): 12825-30.
  • Moudgil R, Menon V, Xu Y, Musat-Marcu S, Kumar D, Jugdutt BI. Postischemic apoptosis and functional recovery after angiotensin II type 1 receptor blockade in isolated working rat hearts. J Hypertens 2001; 19(6): 1121-9.
  • Wu ML, Tsai KL, Wang SM, Wu JC, Wang BS, Lee YT. Mechanism of hydrogen peroxide and hydroxyl free radical- induced intracellular acidification in cultured rat cardiac myoblasts. Circ Res 1996; 78(4): 564-72.
  • Adams JM, Cory S. The Bcl-2 protein family: arbiters of cell survival. Science 1998; 281(5381): 1322-6.
  • Zamzami N, Metivier D, Kroemer G. Quantitation of mitochondrial transmembrane potential in cells and in isolated mitochondria. Methods Enzymol 2000; 322, 208-13.
  • Zhang YW, Shi J, Li YJ, Wei L. Cardiomyocyte death in doxorubicin-induced cardiotoxicity. Arch Immunol Ther Exp (Warsz) 2009; 57(6): 435-45.
  • Vurusaner B, Poli G, Basaga H. Tumor suppressor genes and ROS: complex networks of interactions. Free Radic Biol Med 2012; 52(1): 7-18.
  • Nithipongvanitch R, Ittarat W, Velez JM, Zhao R, St Clair DK, Oberley TD. Evidence for p53 as guardian of the cardiomyocyte mitochondrial genome following acute adriamycin treatment. J Histochem Cytochem 2007; 55(6): 629-39.
  • Tacar O, Sriamornsak P, Dass CR. Doxorubicin: an update on anticancer molecular action, toxicity and novel drug delivery systems. J Pharm Pharmacol 2013; 65(2): 157-70.
  • Lorenzo E, Ruiz-Ruiz C, Quesada AJ, Hernandez G, Rodriguez A, Lopez-Rivas, Redondo JM. Doxorubicin induces apoptosis and CD95 gene expression in human primary endothelial mechanism. J Biol Chem 2002; 277(13): 10883-92. a p53-dependent
  • Narula J, Pandey P, Arbustini E, Haider N, Narula N, Kolodgie FD, Dal Bello B, Semigran MJ, Bielsa-Masdeu A, Dec GW, Israels S, Ballester M, Virmani R, Saxena S, Kharbanda S. Apoptosis in heart failure: release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathy. Proc Natl Acad Sci U S A 1996; 96(14): 8144-9.
  • Nithipongvanitch R, Ittarat W, Cole MP, Tangpong J, Clair DK, Oberley TD. Mitochondrial and nuclear p53 localization in cardiomyocytes: redox modulation by doxorubicin (Adriamycin)? Antioxid Redox Signal 2007; 9(7): 1001-8.
  • Sugden PH, Clerk A. "Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen- activated protein kinases) in the myocardium. Circ Res 1998; 83(4): 345-52.
  • Tsoyi K, Jang HJ, Nizamutdinova IT, Kim YM, Lee YS, Kim HJ, Seo HG, Lee JH, Chang KC.Metformin inhibits HMGB1 release in LPS-treated RAW 264.7 cells and increases survival rate of endotoxaemic mice. Br J Pharmacol 2011; 162(7): 1498-508.
  • Yao Y, Xu X, Zhang G, Zhang Y, Qian W, Rui T. Role of HMGB1 in doxorubicin-induced myocardial apoptosis and its regulation pathway. Basic Res Cardiol 2012; 107(3): 267.
  • Tang D, Kang R, Zeh HJ 3rd, Lotze MT. High-mobility group box 1, oxidative stress, and disease. Antioxid Redox Signal 2011; 14(7): 1315-35.
  • Luo Y, Chihara Y, Fujimoto K, Sasahira T, Kuwada M, Fujiwara R, Fujii K, Ohmori H, Kuniyasu H. High mobility group box 1 released from necrotic cells enhances regrowth and metastasis of cancer cells that have survived chemotherapy. Eur J Cancer 2013; 49(3): 741-51.
  • Yu Y, Xie M, He YL, Xu WQ, Zhu S, Cao LZ. [Role of high mobility group box 1 in adriamycin-induced apoptosis in leukemia K562 cells]. Ai Zheng 2008; 27(9): 929-33.
  • D'Agati V, Schmidt AM. RAGE and the pathogenesis of chronic kidney disease. Nat Rev Nephrol 6(6): 352-60.
  • Zhang Y, Zhang T, Cao CM, Xiao RP. mTOR: good, bad, or ugly? Cardiovasc Res 2012; 95(3): 261-2.
  • Konishi M, Haraguchi G, Ohigashi H, Ishihara T, Saito K, Nakano Y, Isobe M. Adiponectin protects against doxorubicin- induced cardiomyopathy by anti-apoptotic effects through AMPK up-regulation. Cardiovasc Res 2011; 89(2): 309-19.
  • Ahn YJ, Kim H, Lim H, Lee M, Kang Y, Moon S, Kim HS, Kim HH. AMP-activated protein kinase: implications on ischemic diseases. BMB Rep 2012; 45(9): 489-95.
Yıl 2015, Cilt: 1 Sayı: 1, 29 - 33, 15.04.2015

Öz

Kaynakça

  • Wilking N, Jönsson B, Högberg D. "Patient Access to Cancer Drugs http://www.comparatorreports.se/Patient%20Access%20to%2 0Cancer%20Treatment%20in%20Turkey.pdf. Son erişim tarihi: 14 Şubat 2014. Turkey"
  • Minami M, Matsumoto S, Horiuchi H. Cardiovascular side- effects of modern cancer therapy. Circ J 2010; 74, 1779-86.
  • Horacek JM, Vasatova M, Pudil R, Tichy M, Zak P, Jakl M, Jebavy L, Maly J. Biomarkers for the early detection of anthracycline-induced cardiotoxicity: current status. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014; 158 (4): 511-517.
  • Jemal A, Siegel R, Ward E, Murray T, Xu J. Smigal C, Thun M.J. Cancer statistics. CA Cancer J Clin 2006; 56(2):106-30.
  • Bristow MR, Thompson PD, Martin RP, Mason JW, Billingham cardiotoxicity. Am J Med 1978; 65(5): 823-32. Early anthracycline
  • Bleyer WA. The impact of childhood cancer on the United States and the world. CA Cancer J Clin 1990; 40(6): 355-67.
  • Johnson BA, Cheang MS, Goldenberg GJ. Comparison of adriamycin uptake in chick embryo heart and liver cells an murine L5178Y lymphoblasts in vitro: role of drug uptake in cardiotoxicity. Cancer Res1986; 46(1): 218-23.
  • Huber SA. Doxorubicin-induced alterations in cultured myocardial cells stimulate cytolytic T lymphocyte responses. Am J Pathol 1990; 137(2): 449-56.
  • Doroshow JH, Locker GY, Myers CE. Enzymatic defenses of the mouse heart against reactive oxygen metabolites: alterations produced by doxorubicin. J Clin Invest 1980; 65(1): 128-35.
  • Berthiaume JM, Wallace KB. Adriamycin-induced oxidative mitochondrial cardiotoxicity. Cell Biol Toxicol 2007; 23(1): 15- 25.
  • Tokarska-Schlattner M, Zaugg M, Zuppinger C, Wallimann T, Schlattner U. New insights into doxorubicin-induced cardiotoxicity: the critical role of cellular energetics. J Mol Cell Cardiol 2006; 41(3): 389-405.
  • Goormaghtigh E, Huart P, Praet M, Brasseur R, Ruysschaert JM. Structure of the adriamycin-cardiolipin complex. Role in mitochondrial toxicity. Biophys Chem 1990; 35(2): 247-57.
  • Monteiro JP, Oliveira PJ, Jurado AS. Mitochondrial membrane lipid remodeling in pathophysiology: a new target for diet and therapeutic interventions. Prog Lipid Res 2013; 52(4): 513-28.
  • Simunek T, Sterba M, Popelova O, Adamcova M, Hrdina R, Gersl, V. Anthracycline-induced cardiotoxicity: overview of studies examining the roles of oxidative stress and free cellular iron. Pharmacol Rep 2009; 61(1): 154-71.
  • Minotti G, Menna P, Salvatorelli E, Cairo G, Gianni L. Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity. Pharmacol Rev 2004; 56(2): 185-229.
  • Kubasiak LA, Hernandez OM, Bishopric NH, Webster KA. Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3. Proc Natl Acad Sci U S A 2002; 99(20): 12825-30.
  • Moudgil R, Menon V, Xu Y, Musat-Marcu S, Kumar D, Jugdutt BI. Postischemic apoptosis and functional recovery after angiotensin II type 1 receptor blockade in isolated working rat hearts. J Hypertens 2001; 19(6): 1121-9.
  • Wu ML, Tsai KL, Wang SM, Wu JC, Wang BS, Lee YT. Mechanism of hydrogen peroxide and hydroxyl free radical- induced intracellular acidification in cultured rat cardiac myoblasts. Circ Res 1996; 78(4): 564-72.
  • Adams JM, Cory S. The Bcl-2 protein family: arbiters of cell survival. Science 1998; 281(5381): 1322-6.
  • Zamzami N, Metivier D, Kroemer G. Quantitation of mitochondrial transmembrane potential in cells and in isolated mitochondria. Methods Enzymol 2000; 322, 208-13.
  • Zhang YW, Shi J, Li YJ, Wei L. Cardiomyocyte death in doxorubicin-induced cardiotoxicity. Arch Immunol Ther Exp (Warsz) 2009; 57(6): 435-45.
  • Vurusaner B, Poli G, Basaga H. Tumor suppressor genes and ROS: complex networks of interactions. Free Radic Biol Med 2012; 52(1): 7-18.
  • Nithipongvanitch R, Ittarat W, Velez JM, Zhao R, St Clair DK, Oberley TD. Evidence for p53 as guardian of the cardiomyocyte mitochondrial genome following acute adriamycin treatment. J Histochem Cytochem 2007; 55(6): 629-39.
  • Tacar O, Sriamornsak P, Dass CR. Doxorubicin: an update on anticancer molecular action, toxicity and novel drug delivery systems. J Pharm Pharmacol 2013; 65(2): 157-70.
  • Lorenzo E, Ruiz-Ruiz C, Quesada AJ, Hernandez G, Rodriguez A, Lopez-Rivas, Redondo JM. Doxorubicin induces apoptosis and CD95 gene expression in human primary endothelial mechanism. J Biol Chem 2002; 277(13): 10883-92. a p53-dependent
  • Narula J, Pandey P, Arbustini E, Haider N, Narula N, Kolodgie FD, Dal Bello B, Semigran MJ, Bielsa-Masdeu A, Dec GW, Israels S, Ballester M, Virmani R, Saxena S, Kharbanda S. Apoptosis in heart failure: release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathy. Proc Natl Acad Sci U S A 1996; 96(14): 8144-9.
  • Nithipongvanitch R, Ittarat W, Cole MP, Tangpong J, Clair DK, Oberley TD. Mitochondrial and nuclear p53 localization in cardiomyocytes: redox modulation by doxorubicin (Adriamycin)? Antioxid Redox Signal 2007; 9(7): 1001-8.
  • Sugden PH, Clerk A. "Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen- activated protein kinases) in the myocardium. Circ Res 1998; 83(4): 345-52.
  • Tsoyi K, Jang HJ, Nizamutdinova IT, Kim YM, Lee YS, Kim HJ, Seo HG, Lee JH, Chang KC.Metformin inhibits HMGB1 release in LPS-treated RAW 264.7 cells and increases survival rate of endotoxaemic mice. Br J Pharmacol 2011; 162(7): 1498-508.
  • Yao Y, Xu X, Zhang G, Zhang Y, Qian W, Rui T. Role of HMGB1 in doxorubicin-induced myocardial apoptosis and its regulation pathway. Basic Res Cardiol 2012; 107(3): 267.
  • Tang D, Kang R, Zeh HJ 3rd, Lotze MT. High-mobility group box 1, oxidative stress, and disease. Antioxid Redox Signal 2011; 14(7): 1315-35.
  • Luo Y, Chihara Y, Fujimoto K, Sasahira T, Kuwada M, Fujiwara R, Fujii K, Ohmori H, Kuniyasu H. High mobility group box 1 released from necrotic cells enhances regrowth and metastasis of cancer cells that have survived chemotherapy. Eur J Cancer 2013; 49(3): 741-51.
  • Yu Y, Xie M, He YL, Xu WQ, Zhu S, Cao LZ. [Role of high mobility group box 1 in adriamycin-induced apoptosis in leukemia K562 cells]. Ai Zheng 2008; 27(9): 929-33.
  • D'Agati V, Schmidt AM. RAGE and the pathogenesis of chronic kidney disease. Nat Rev Nephrol 6(6): 352-60.
  • Zhang Y, Zhang T, Cao CM, Xiao RP. mTOR: good, bad, or ugly? Cardiovasc Res 2012; 95(3): 261-2.
  • Konishi M, Haraguchi G, Ohigashi H, Ishihara T, Saito K, Nakano Y, Isobe M. Adiponectin protects against doxorubicin- induced cardiomyopathy by anti-apoptotic effects through AMPK up-regulation. Cardiovasc Res 2011; 89(2): 309-19.
  • Ahn YJ, Kim H, Lim H, Lee M, Kang Y, Moon S, Kim HS, Kim HH. AMP-activated protein kinase: implications on ischemic diseases. BMB Rep 2012; 45(9): 489-95.
Toplam 37 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Bölüm Araştırma Makalesi
Yazarlar

Celal Güven Bu kişi benim

Eylem Taşkın

Yayımlanma Tarihi 15 Nisan 2015
Gönderilme Tarihi 15 Mart 2016
Yayımlandığı Sayı Yıl 2015 Cilt: 1 Sayı: 1

Kaynak Göster

AMA Güven C, Taşkın E. Adriyamisinin Neden olduğu Kalp Yetmezliğinde HMGB-1 ve AMPK’nin Olası Etkileri. ADYÜ Sağlık Bilimleri Derg. Nisan 2015;1(1):29-33.