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Cardiovascular Research Advance Access originally published online on July 11, 2008
Cardiovascular Research 2008 79(4):547-548; doi:10.1093/cvr/cvn191
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Proteasome inhibition and stress compromise the heart in chemotherapy

Yolande E.A. Appelman1 and Pieter A. Doevendans2,*

1 Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands
2 Department of Cardiology, University Medical Center Utrecht, PO Box 85500, GA Utrecht 3508, The Netherlands

* Corresponding author. +31 88 755 9801; fax: +31 30 254 2155. E-mail address: p.doevendans@umcutrecht.nl

This editorial refers to ‘Overexpression of endoplasmic reticulum-resident chaperone attenuates cardiomyocyte death induced by proteasome inhibition’ by H.Y. Fu et al.,6 pp. 600–610, this issue.

The first 10% of the full text of this article appears below.

Several new therapeutic options are opening up for the treatment of haematological and solid malignancies. Although the effects on the malignancies can be dramatic, the collateral damage can be devastating as well. The concept of gene therapy was to develop cell-type-specific techniques, and similar expectations were raised with the concept of targeting cells specifically by binding selected receptors or other proteins. Yet, most therapies that have reached the clinic are not specific and will therefore influence all tissues and organs. This will make the heart a vulnerable organ, as it has limited or no regenerative capacity.

The . . . [Full Text of this Article]


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Overexpression of endoplasmic reticulum-resident chaperone attenuates cardiomyocyte death induced by proteasome inhibition
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Cardiovasc Res 2008 79: 600-610. [Abstract] [Full Text] [PDF]



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