Apoptosis myocardial infarction

AT2 receptors are present at high density in all tissues during fetal development, but they are much less abundant in the adult where they are expressed at high concentration only in the adrenal medulla, reproductive tissues, vascular endothelium, and parts of the brain. AT2 receptors are up-regulated in pathologic conditions including heart failure and myocardial infarction. The functions of the AT2 receptor appear to include fetal tissue development, inhibition of growth and proliferation, cell differentiation, apoptosis, and vasodilation. [Pg.377]

S100B Overexpression Female specific hyperactivity, lack of habituation to novelty, reduced T-maze spontaneous alternation rate, abnormal exploratory behavior Enhanced astrocytosis and neurite proliferation Impaired learning and memory, increased dendrite density, enhanced age-related loss of dendrites Inhibitory effect on cardiac hypertrophy Increased susceptibility to hypoxia-ischemia Increased apoptosis after myocardial infarction Enhanced neuroinflammation and neuronal dysfunction induced by amyloid-(3... [Pg.101]

Knock-out Increased synaptic plasticity, spatial memory and fear memory Chronic gliosis Decreased susceptibility to hypoxia-ischemia Enhanced epileptogenesis Enhanced Ca2+ transients Enhanced hypertrophy, decreased apoptosis and improved hemodynamics after myocardial infarction... [Pg.101]

Quin, F., Yan, C., Patel, R., Liu, W., and Dong, E. 2006. Vitamin C and E attenuate apoptosis, p-adrenergic receptor desensitization, and sarcoplasmic reticular Ca2+ ATPase dowmegulation after myocardial infarction. Free Radic. Biol. Med. 40 1827-1842. [Pg.174]

The discovery of apoptosis sheds a new light on the role of cell death in myocardial infarction and other cardiovascular diseases. There is mounting evidence that apoptosis plays an important role at multiple points in the evolution of myocardial infarction, and comprises not only cardiomyocytes but also inflammatory cells, as well as cells of granulation tissue and... [Pg.10]

Takemura G, Fujiwara H. Role of apoptosis in remodeling after myocardial infarction. Pharmacol Ther 2004 104 1-16. [Pg.33]

Bardales RH, Hailey LS, Xie SS, Schaefer RF, Hsu SM. In situ apoptosis assay for the detection of early acute myocardial infarction. Am J Pathol 1996 149 821-829. [Pg.38]

Saraste A, Pulkki K, Kallajoki M, Henriksen K, Parvinen M, Voipio-Pulkki LM. Apoptosis in human acute myocardial infarction. Circulation 1997 95 320-323. [Pg.38]

Veinot JP, Gattinger DA, Fliss H. Early apoptosis in human myocardial infarcts. Hum Pathol 1997 28 485-492. [Pg.38]

Toyoda Y, Shida T, Wakita N, Ozaki N, Takahashi R, Okada M. Evidence of apoptosis induced by myocardial ischemia A case of ventricular septal rupture following acute myocardial infarction. Cardiology 1998 90 149-151. [Pg.38]

Piro FR, di Gioia CR, Gallo P, Giordano C, d Amati G. Is apoptosis a diagnostic marker of acute myocardial infarction Arch Pathol Lab Med 2000 124 827-831. [Pg.38]

Abbate A, Bussani R, Biondi-Zoccai GG, Rossiello R, Silvestri F, Baldi F, et al. Persistent infarct-related artery occlusion is associated with an increased myocardial apoptosis at post-mortem examination in humans late after an acute myocardial infarction. Circulation 2002 106 1051-1054. [Pg.39]

Sam F, Sawyer DB, Chang DL, Eberli FR, Ngoy S, Jain M, et al. Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart. Am J Physiol Heart Circ Physiol 2000 279 H422-H428. [Pg.40]

Schwarz K, Simonis G, Yu X, Wiedemann S, Strasser RH. Apoptosis at a distance Remote activation of caspase-3 occurs early after myocardial infarction. Mol Cell Biochem 2006 281 45-54. [Pg.40]

Oskarsson HJ, Coppey L, Weiss RM, Li WG. Antioxidants attenuate myocyte apoptosis in the remote non-infarcted myocardium following large myocardial infarction. Cardio-vasc Res 2000 45 679-687. [Pg.40]

Hayakawa K, Takemura G, Kanoh M, Li Y, Koda M, Kawase Y, et al. Inhibition of granulation tissue cell apoptosis during the subacute stage of myocardial infarction improves cardiac remodeling and dysfunction at the chronic stage. Circulation 2003 108 104-109. [Pg.40]

Chandrashekhar Y, Sen S, Anway R, Shuros A, Anand I. Long-term caspase inhibition ameliorates apoptosis, reduces myocardial troponin-1 cleavage, protects left ventricular function, and attenuates remodeling in rats with myocardial infarction. J Am Coll Cardiol 2004 43 295-301. [Pg.40]

Takemura G, Ohno M, Hayakawa Y, Misao J, Kanoh M, Ohno A, et al. Role of apoptosis in the disappearance of infiltrated and proliferated interstitial cells after acute myocardial infarction. Circ Res 1998 82 1130-1138. [Pg.41]

Yaoita H, Ogawa K, Maehara K, Maruyama Y. Apoptosis in relevant clinical situations Contribution of apoptosis in myocardial infarction. Cardiovasc Res 2000 45 630-641. [Pg.41]

The family of cysteine proteases, which are called caspases, plays a major role in the execution of apoptotic cell death (12). Many studies suggest that increased apoptosis and caspase activity contribute to tissue damage in both acute (e.g., myocardial infarction, stroke, sepsis, spinal cord injury) and chronic (e.g., Alzheimer s, Parkinson s, Huntington s disease) human diseases (13,14). Caspase family members are also prominently... [Pg.169]

Z.Q. Zhao, C.D. Morris, J.M. Budde, N.P. Wang, S. Muraki, H.Y. Sun and R.A. Guyton, Inhibition of myocardial apoptosis reduces infarct size and improves regional contractile dysfunction during reperfusion, Cardiovasc Res. 59(1), 132-142 (2003). [Pg.65]

Y. Ruixing, Y. Dezhai, and L. Jiaquan, Effects of cardiotrophin-1 on hemodynamics and cardiomyocyte apoptosis in rats with acute myocardial infarction, J Med Invest 51, 29-37 (2004). [Pg.166]

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