Ишемическое посткондиционирование сердца. Часть III

Ишемическое посткондиционирование сердца. Часть III

Автор: Маслов Л.Н., Лишманов Ю.Б.

Журнал: Сибирский журнал клинической и экспериментальной медицины @cardiotomsk

Рубрика: Обзоры и лекции

Статья в выпуске: 1 т.28, 2013 года.

Бесплатный доступ

Авторы обзора анализируют данные о том, что G-белоксопряженные рецепторы, фосфатидилинозитол-3-киназа, Aktкиназа, эндотелиальная NO-синтаза, гуанилатциклаза, цГМФ, протеинкиназа G, митохондриальная протеинкиназа Сƒ, митохондриальные АТФ-чувствительные К+каналы, активные формы кислорода, поры, регулирующие проницаемость митохондрий, участвуют в сигнальном каскаде посткондиционирования.

Сердце, ишемическое посткондиционирование, сигнальный каскад

Короткий адрес: https://sciup.org/14919825

IDR: 14919825

Список литературы Ишемическое посткондиционирование сердца. Часть III

  • Маслов Л.Н. Новые подходы к профилактике и терапии ишемических и реперфузионных повреждений сердца при остром инфаркте миокарда//Сибирский медицинский журнал (Томск). -2010. -Т. 25, № 2, вып. 1. -С. 17-24.
  • Argaud L., GateauRoesch O., Raisky O. et al. Postconditioning inhibits mitochondrial permeability transition//Circulation. -2005. -Vol. 111 (2). -P. 194-197.
  • Baines C.P., Song C.X., Zheng Y.T. et al. Protein kinase Cе interacts with and inhibits the permeability transition pore in cardiac mitochondria//Circ. Res. -2003. -Vol. 92 (8). -P. 873-880.
  • Bopassa J.C., Ferrera R., GateauRoesch O. et al. PI 3kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning//Cardiovasc. Res. -2006. -Vol. 69 (1). -P. 178-185.
  • Churchill E.N., Szweda L.I. Translocation of PKC to mitochondria during cardiac reperfusion enhances superoxide anion production and induces loss in mitochondrial function//Arch. Biochem. Biophys. -2005. -Vol. 439 (2). -P. 194-199.
  • Costa A.D., Garlid K.D., West I.C. et al. Protein kinase G transmits the cardioprotective signal from cytosol to mitochondria//Circ. Res. -2005. -Vol. 97 (4). -P. 329-336.
  • Costa A.D., Jakob R., Costa C.L. et al. The mechanism by which the mitochondrial ATPsensitive K+ channel opening and H2O2 inhibit the mitochondrial permeability transition//J. Biol. Chem. -2006. -Vol. 281 (30). -P. 20801-20808.
  • Costa A.D., Pierre S.V., Cohen M.V. et al. cGMP signalling in pre and postconditioning: the role of mitochondria//Cardiovasc. Res. -2008. -Vol. 77 (2). -P. 344-352.
  • Darling C.E., Jiang R., Maynard M. et al. Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2//Am. J. Physiol. Heart Circ. Physiol. -2005. -Vol. 289 (4). -P. H1618-H1626.
  • GateauRoesch O., Argaud L., Ovize M. Mitochondrial permeability transition pore and postconditioning//Cardiovasc. Res. -2006. -Vol. 70 (2). -P. 264-273.
  • Griffiths E.J., Halestrap A.P. Mitochondrial nonspecific pores remain closed during cardiac ischaemia, but open upon reperfusion//Biochem J. -1995. -Vol. 307 (1). -P. 93-98.
  • Hausenloy D.J., Maddock H.L., Baxter G.F. et al. Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?//Cardiovasc. Res. -2002. -Vol. 55 (3). -P. 534-543.
  • Hausenloy D.J., Yellon D.M. Preconditioning and postconditioning: united at reperfusion//Pharmacol. Ther. -2007. -Vol. 116 (2). -P. 173-191.
  • Inagaki K., Chen L., Ikeno F. et al. Inhibition of protein kinase C protects against reperfusion injury of the ischemic heart in vivo//Circulation. -2003a. -Vol. 108 (19). -P. 2304-2307.
  • Inagaki K., Hahn H.S., Dorn G.W. et al. Additive protection of the ischemic heart ex vivo by combined treatment with protein kinase C inhibitor and protein kinase C activator//Circulation. -2003b. -Vol. 108 (7). -P. 869-875.
  • Kostyak J.C., Hunter J.C., Korzick D.H. Acute PKC inhibition limits ischaemiareperfusion injury in the aged rat heart: role of GSK3//Cardiovasc. Res. -2006. -Vol. 70. (2). -P. 325-334.
  • Kroemer G., Galluzzi L., Brenner C. Mitochondrial membrane permeabilization in cell death//Physiol. Rev. -2007. -Vol. 87 (1). -P. 99-163.
  • Kuno A., Solenkova N.V., Solodushko V. et al. Infarct limitation by a protein kinase G activator at reperfusion in rabbit hearts is dependent on sensitizing the heart to A2b agonists by protein kinase C//Am. J. Physiol. Heart Circ. Physiol. -2008. -Vol. 295 (3). -P. H1288-H1295.
  • Murriel C.L., Churchill E., Inagaki K. et al. Protein kinase C activation induces apoptosis in response to cardiac ischemia and reperfusion damage: a mechanism involving BAD and the mitochondria//J. Biol. Chem. -2004. -Vol. 279 (46). -P. 47985-47991.
  • Oldenburg O., Qin Q., Krieg T. et al. Bradykinin induces mitochondrial ROS generation via NO, cGMP, PKG, and mitoKATP channel opening and leads to cardioprotection//Am. J. Physiol. -2004. -Vol. 286 (1). -P. H468-H476.
  • Schwartz L.M, Lagranha C.J. Ischemic postconditioning during reperfusion activates Akt and ERK without protecting against lethal myocardial ischemiareperfusion injury in pigs//Am. J. Physiol. Heart Circ. Physiol. -2006. -Vol. 290 (3). -P. H1011-H018.
  • Sun H.Y., Wang N.P., Halkos M. et al. Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen activated protein kinase signaling pathways//Apoptosis. -2006. -Vol. 11 (9). -P. 1583-1593.
  • Tsang A., Hausenloy D.J., Mocanu M.M. et al. Postconditioning: a form of "modified reperfusion" protects the myocardium by activating the phosphatidylinositol 3kinaseAkt pathway//Circ. Res. -2004. -Vol. 95 (3). -P. 230-232.
  • VintenJohansen J., Zhao Z.Q., Zatta A.J. et al. Postconditioning -a new link in nature's armor against myocardial ischemia reperfusion injury//Basic Res. Cardiol. -2005. -Vol. 100 (4). -P. 295-310.
  • Wang C., Neff D.A., Krolikowski J.G. et al. The influence of B cell lymphoma 2 protein, an antiapoptotic regulator of mitochondrial permeability transition, on isofluraneinduced and ischemic postconditioning in rabbits//Anesth. Analg. -2006. -Vol. 102 (5). -P. 1355-1360.
  • Yang X.M., Krieg T., Cui L. et al. NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO//J. Mol. Cell. Cardiol. -2004a. -Vol. 36 (3). -P. 411-421.
  • Yang X.M., Proctor J.B., Cui L. et al. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways//J. Am. Coll. Cardiol. -2004b. -Vol. 44 (5). -P. 1103-1110.
  • Yang X.M., Philipp S., Downey J.M. et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3kinase and guanylyl cyclase activation//Basic Res. Cardiol. -2005. -Vol. 100 (1). -P. 57-63.
  • Yellon D.M., Downey J.M. Preconditioning the myocardium: from cellular physiology to clinical cardiology//Physiol. Rev. -2003. -Vol. 83 (4). -P. 1113-1151.
  • Zatta A.J., Kin H., Lee G. et al. Infarctsparing effect of myocardial postconditioning is dependent on protein kinase C signalling//Cardiovasc. Res. -2006. -Vol. 70 (2). -P. 315-324.
  • Zhao Z.Q., Sun H.Y., Wang N.P. et al. Hypoxic postconditioning attenuates cardiomyocyte apoptosis via inhibition JNK and p38 kinases pathway//J. Mol. Cell. Cardiol. -2005. -Vol. 38 (5). -P. 870.
  • Zhao Z.Q., VintenJohansen J. Postconditioning: reduction of reperfusioninduced injury//Cardiovasc. Res. -2006. -Vol. 70 (2). -P. 200-211.
  • Zhu M., Feng J., Lucchinetti E. et al. Ischemic postconditioning protects remodeled myocardium via the PI3KPKB/Akt reperfusion injury salvage kinase pathway//Cardiovasc. Res. -2006. -Vol. 72 (1). -P. 152-162.
Еще
Статья научная
QR-код для установки приложения SciUp Наведите камеру и скачайте бесплатное приложение SciUp