Zobrazeno 1 - 10
of 56
pro vyhledávání: '"Peter Razeghi"'
Publikováno v:
Current Problems in Cardiology. 33:163-196
Cardiovascular disease is commonly found in cancer patients. The co-existence of heart disease and cancer in a patient often complicates treatment, because therapy for one disease may negatively affect the outcome of the other disease. In addition, g
Autor:
Peter Razeghi, Stanislaw M. Stepkowski, Mou Er Wang, Keith A. Youker, Heinrich Taegtmeyer, Leonard Golfman
Publikováno v:
Cardiovascular Research. 74:133-139
Unloading of the rodent heart activates the fetal gene program, decreases peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARalpha-regulated gene expression (MCAD), and induces cardiomyocyte atrophy. NF-kappaB regulates the fetal ge
Autor:
Heinrich Taegtmeyer, Peter Razeghi
Publikováno v:
Annals of the New York Academy of Sciences. 1080:110-119
The size of a cardiomyocyte is determined by relative rates of protein synthesis and degradation. Signaling pathways regulating myocardial protein synthesis have been extensively investigated, not the least because in patients hypertrophy increases c
Autor:
M. Faadiel Essop, Saumya Sharma, Martin E. Young, Heinrich Taegtmeyer, Stanislaw M. Stepkowski, Kedryn K. Baskin, Peter Razeghi
Publikováno v:
Biochemical and Biophysical Research Communications. 342:361-364
Background In skeletal muscle, transcript levels of proteins regulating the ubiquitin proteasome system (UPS) increase with atrophy and decrease with hypertrophy. Whether the same is true for heart muscle is not known. Aim of the study We set out to
Autor:
Marco Sandri, Kenneth Walsh, Peter Razeghi, Henrike Maatz, Yasuhiro Izumiya, David R. Pimentel, Ling Zeng, Alfred L. Goldberg, Heinrich Taegtmeyer, Stewart H. Lecker, Kaori Sato, Stephan Schiekofer, Ichiro Shiojima, Carsten Skurk
Publikováno v:
Journal of Biological Chemistry. 280:20814-20823
Although signaling mechanisms inducing cardiac hypertrophy have been extensively studied, little is known about the mechanisms that reverse cardiac hypertrophy. Here, we describe the existence of a similar Akt/forkhead signaling axis in cardiac myocy
Autor:
Martin E. Young, Christopher J. McLeod, Peter Razeghi, Michael N. Sack, Heinrich Taegtmeyer, M. Faadiel Essop
Publikováno v:
Biochemical and Biophysical Research Communications. 314:561-564
Mitochondrial uncoupling proteins 2 and 3 (UCP2 and UCP3) are postulated to contribute to antioxidant defense, nutrient partitioning, and energy efficiency in the heart. To distinguish isotype function in response to metabolic stress we measured card
Autor:
Mark L. Entman, Brian A. Bruckner, George P. Noon, Heinrich Taegtmeyer, Javier A. Lafuente, Sonny S. Stetson, O.H. Frazier, Peter Razeghi, Larry O. Thompson, Keith A. Youker, Matthias Loebe
Publikováno v:
The Journal of Heart and Lung Transplantation. 23:36-42
There have been increasing reports of cardiac improvement in heart failure patients supported by left ventricular assist devices (LVADs i.e.), including a number of patients who have tolerated removal of the device without the benefit of cardiac tran
Autor:
Peter Razeghi, Stanislaw M. Stepkowski, Heinrich Taegtmeyer, Jun Ying, Yi-Ping Li, Saumya Sharma, Michael B. Reid
Publikováno v:
Circulation. 108:2536-2541
Background— Mechanical unloading of the heart results in atrophic remodeling. In skeletal muscle, atrophy is associated with inactivation of the mammalian target of rapamycin (mTOR) pathway and upregulation of critical components of the ubiquitin p
Autor:
Heinrich Taegtmeyer, M. Faadiel Essop, Nayna Manga, Shahrzad Abbasi, Janice M. Huss, Peter Razeghi
Publikováno v:
Biochemical and Biophysical Research Communications. 303:1024-1027
Cardiac hypertrophy and atrophy increase expression of fetal iso-genes. A common factor is a decrease in cellular oxygen tension. To test the hypothesis that hypoxia changes cardiac MHC iso-gene expression Wistar rats were exposed to 24 and 48 h of h
Autor:
Peter Razeghi, Saumya Sharma, Heinrich Taegtmeyer, Keith A. Youker, Brian A. Bruckner, O.H. Frazier
Publikováno v:
Cardiology. 100:17-22
Background: Left ventricular assist device (LVAD) support of the failing human heart improves myocyte function and increases cell survival. One potential mechanism underlying this phenomenon is activation of the protein kinase B (PKB)/Akt/glycogen sy