Metallothionein alleviates cardiac dysfunction in streptozotocin-induced diabetes: role of Ca2+ cycling proteins, NADPH oxidase, poly(ADP-Ribose) polymerase and myosin heavy chain isozyme.

[1]  W. Dillmann.  Diabetes Mellitus Induces Changes in Cardiac Myosin of the Rat , 1980, Diabetes.

[2]  E. Blough,et al.  Enhanced electrophoretic separation and resolution of myosin heavy chains in mammalian and avian skeletal muscles. , 1996, Analytical biochemistry.

[3]  C. Ballard-Croft,et al.  Mechanisms underlying depressed Na+/Ca2+ exchanger activity in the diabetic heart. , 1997, Cardiovascular research.

[4]  A. Davidoff,et al.  Diabetes rapidly induces contractile dysfunctions in isolated ventricular myocytes. , 1997, The American journal of physiology.

[5]  Peter J Reiser,et al.  Electrophoretic separation and quantitation of cardiac myosin heavy chain isoforms in eight mammalian species. , 1998, American journal of physiology. Heart and circulatory physiology.

[6]  D. Talwar,et al.  Dietary flavonols protect diabetic human lymphocytes against oxidative damage to DNA. , 1999, Diabetes.

[7]  A. Bode,et al.  Altered cardiac excitation-contraction coupling in ventricular myocytes from spontaneously diabetic BB rats. , 2000, American journal of physiology. Heart and circulatory physiology.

[8]  H. Taegtmeyer,et al.  Streptozotocin-induced changes in cardiac gene expression in the absence of severe contractile dysfunction. , 2000, Journal of molecular and cellular cardiology.

[9]  L. Wold,et al.  IGF-I attenuates diabetes-induced cardiac contractile dysfunction in ventricular myocytes. , 2002, American journal of physiology. Endocrinology and metabolism.

[10]  D. Bers.  Cardiac excitation–contraction coupling , 2002, Nature.

[11]  N. Narula,et al.  Apoptosis in heart failure represents programmed cell survival, not death, of cardiomyocytes and likelihood of reverse remodeling. , 2002, Journal of cardiac failure.

[12]  Jun Ren,et al.  Impaired cardiac function and IGF-I response in myocytes from calmodulin-diabetic mice: role of Akt and RhoA. , 2003, American journal of physiology. Endocrinology and metabolism.

[13]  L. Wold,et al.  Increases in insulin-like growth factor-1 level and peroxidative damage after gestational ethanol exposure in rats. , 2003, Pharmacological research.

[14]  Jun Ren,et al.  Metallothionein prevents diabetes-induced deficits in cardiomyocytes by inhibiting reactive oxygen species production. , 2003, Diabetes.

[15]  L. Wold,et al.  AT1 Blockade Prevents Glucose-Induced Cardiac Dysfunction in Ventricular Myocytes: Role of the AT1 Receptor and NADPH Oxidase , 2003, Hypertension.

[16]  C. Szabó,et al.  Poly(ADP-Ribose) Polymerase Contributes to the Development of Myocardial Infarction in Diabetic Rats and Regulates the Nuclear Translocation of Apoptosis-Inducing Factor , 2004, Journal of Pharmacology and Experimental Therapeutics.

[17]  P. D. de Tombe,et al.  Depressed cardiac tension cost in experimental diabetes is due to altered myosin heavy chain isoform expression. , 2004, American journal of physiology. Heart and circulatory physiology.

[18]  G. Biolo,et al.  Myostatin expression is not altered by insulin deficiency and replacement in streptozotocin-diabetic rat skeletal muscles. , 2004, Clinical nutrition.

[19]  Jun Ren,et al.  Overexpression of Aldehyde Dehydrogenase-2 (ALDH2) Transgene Prevents Acetaldehyde-induced Cell Injury in Human Umbilical Vein Endothelial Cells , 2004, Journal of Biological Chemistry.

[20]  Xueliang Du,et al.  Role of oxygen derived radicals for vascular dysfunction in the diabetic heart: Prevention by α-tocopherol? , 1998, Molecular and Cellular Biochemistry.

[21]  P. Anversa,et al.  Transgenic overexpression of insulin-like growth factor I prevents streptozotocin-induced cardiac contractile dysfunction and beta-adrenergic response in ventricular myocytes. , 2004, The Journal of endocrinology.

[22]  L. Wold,et al.  Streptozotocin directly impairs cardiac contractile function in isolated ventricular myocytes via a p38 map kinase-dependent oxidative stress mechanism. , 2004, Biochemical and biophysical research communications.

[23]  L. Wold,et al.  Depressed contractile function and adrenergic responsiveness of cardiac myocytes in an experimental model of Parkinson disease, the MPTP-treated mouse , 2004, Neurobiology of Aging.

[24]  F. Recchia,et al.  Role of oxidative-nitrosative stress and downstream pathways in various forms of cardiomyopathy and heart failure. , 2005, Current vascular pharmacology.

[25]  L. Cai,et al.  Inhibition of superoxide generation and associated nitrosative damage is involved in metallothionein prevention of diabetic cardiomyopathy. , 2005, Diabetes.

[26]  N. Metreveli,et al.  Cardiomyocyte defects in diabetic models and protection with cardiac-targeted transgenes. , 2005, Methods in molecular medicine.

[27]  P. D. de Tombe,et al.  Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kinetics. , 2005, American journal of physiology. Heart and circulatory physiology.

[28]  C. Szabó.  Cardioprotective effects of poly(ADP-ribose) polymerase inhibition. , 2005, Pharmacological research.

[29]  C. Fang,et al.  Metallothionein alleviates cardiac contractile dysfunction induced by insulin resistance: role of Akt phosphorylation, PTB1B, PPARγ and c-Jun , 2005, Diabetologia.

[30]  L. Wold,et al.  Oxidative stress and stress signaling: menace of diabetic cardiomyopathy , 2005, Acta Pharmacologica Sinica.

[31]  A. Ceylan-isik,et al.  High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus. , 2006, Journal of applied physiology.

[32]  A. Ceylan-isik,et al.  Diabetic cardiomyopathy , 2004, Endocrine.

[33]  L. Cai,et al.  Oxidative stress and diabetic cardiomyopathy , 2007, Cardiovascular Toxicology.