Myostatin expression in ventricular myocardium in a rat model of volume‐overload heart failure

Background  Mechanical stress increases myocardial myostatin expression. However, the expression of myostatin in chronic heart failure resulting from volume‐overload and after treatment with β‐blockers is little known. The authors hypothesize that myostatin plays a role in the failing myocardium because of volume‐overload.

[1]  W. Aronow Epidemiology, Pathophysiology, Prognosis, and Treatment of Systolic and Diastolic Heart Failure , 2006, Cardiology in review.

[2]  Wei-Shiung Yang,et al.  Insulin-like growth factor-1 mediates stretch-induced upregulation of myostatin expression in neonatal rat cardiomyocytes. , 2005, Cardiovascular research.

[3]  K. Shyu,et al.  Temporal and spatial expression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in a rat model of myocardial ischemia with or without reperfusion. , 2005, Journal of the Formosan Medical Association = Taiwan yi zhi.

[4]  K. Shyu,et al.  Carvedilol modulates the expression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in a rat model of volume-overload heart failure. , 2005, Journal of cardiac failure.

[5]  M. Reiter Cardiovascular drug class specificity: β-blockers , 2004 .

[6]  S. Vanni,et al.  Different Growth Factor Activation in the Right and Left Ventricles in Experimental Volume Overload , 2004, Hypertension.

[7]  M. Reiter Cardiovascular drug class specificity: beta-blockers. , 2004, Progress in cardiovascular diseases.

[8]  M. Kitakaze,et al.  Changes in myocardial gene expression associated with β-blocker therapy in patients with chronic heart failure , 2003 .

[9]  S. Cook,et al.  Transcriptional Effects of Chronic Akt Activation in the Heart* , 2002, The Journal of Biological Chemistry.

[10]  T. Zimmers,et al.  Induction of Cachexia in Mice by Systemically Administered Myostatin , 2002, Science.

[11]  R. Quaife,et al.  Myocardial gene expression in dilated cardiomyopathy treated with beta-blocking agents. , 2002, The New England journal of medicine.

[12]  R. Vulapalli,et al.  Loss of cardiac sympathetic neurotransmitters in heart failure and NE infusion is associated with reduced NGF. , 2002, American journal of physiology. Heart and circulatory physiology.

[13]  Se-Jin Lee,et al.  Regulation of myostatin activity and muscle growth , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[14]  P. Choong,et al.  Myostatin, insulin‐like growth factor‐1, and leukemia inhibitory factor mRNAs are upregulated in chronic human disuse muscle atrophy , 2001, Muscle & nerve.

[15]  R. Dietz,et al.  Differential regulation of cardiac ANP and BNP mRNA in different stages of experimental heart failure. , 2000, American journal of physiology. Heart and circulatory physiology.

[16]  M. Esler,et al.  Reduced myocardial nerve growth factor expression in human and experimental heart failure. , 2000, Circulation research.

[17]  K. Matthews,et al.  Myostatin, a transforming growth factor‐β superfamily member, is expressed in heart muscle and is upregulated in cardiomyocytes after infarct , 1999, Journal of cellular physiology.

[18]  S. Arver,et al.  Organization of the human myostatin gene and expression in healthy men and HIV-infected men with muscle wasting. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[19]  Se-Jin Lee,et al.  Double muscling in cattle due to mutations in the myostatin gene. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[20]  Se-Jin Lee,et al.  Regulation of skeletal muscle mass in mice by a new TGF-p superfamily member , 1997, nature.

[21]  K. Pennert,et al.  Reversal of left ventricular hypertrophy in hypertensive patients. A metaanalysis of 109 treatment studies. , 1992, American journal of hypertension.

[22]  R. Garcia,et al.  Simple, rapid, and effective method of producing aortocaval shunts in the rat. , 1990, Cardiovascular research.