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The Feinstein Institute for Medical Research, The Albert Einstein School of Medicine, Department of Medicine, The Long Island Jewish Medical Center, 270-05 76th Ave, Room B-387, New Hyde Park, NY 11042
(Email: spowell@lij.edu).
| The first 20% of the full text of this article appears below. |
To the Editor:
I read with great interest the article by Stansfield and coworkers [1] that reports observations suggesting that pretreatment of mice with the proteasome inhibitor, PS-519, decreases postischemic infarct size and preserves cardiac function through a mechanism that might be linked to changes in nuclear factor kappa B (NF
B) signaling. Considering the critical role of the ubiquitin proteasome system in cardiac pathophysiology [2], this is an important study; however, certain issues with the experimental design, as well as interpretation of these studies require comment. There is concern that simply showing changes in I
B levels and phosphorylation of
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Ann. Thorac. Surg. 2008 85: 1504.
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S. R. Powell and A. Divald The ubiquitin-proteasome system in myocardial ischaemia and preconditioning Cardiovasc Res, January 15, 2010; 85(2): 303 - 311. [Abstract] [Full Text] [PDF] |
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W. E. Stansfield and C. H. Selzman Reply Ann. Thorac. Surg., April 1, 2008; 85(4): 1504 - 1504. [Full Text] [PDF] |
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