Abstract:
:Heart failure is a leading cause of hospitalization worldwide. No major significant improvements in prognosis have been achieved for heart failure over the last several decades despite advances in disease management. Heart failure itself represents a final common endpoint for several disease entities, including hypertension and coronary artery disease. On a molecular level, certain biochemical features remain common to failing myocardium. Among these are alterations in the β-adrenergic receptor (β-AR) signaling cascade. Recent advances in transgenic and gene therapy techniques have presented novel therapeutic strategies for management of heart failure via genetic manipulation of β-AR signaling including the targeted inhibition of the β-AR kinase (βARK1 or GRK2). In this review, we will discuss the β-AR signaling changes that accompany heart failure as well as corresponding therapeutic strategies. We will then review the evidence from transgenic mouse work supporting the use of β-AR manipulation in the failing heart and more recent in vivo applications of gene therapy directed at reversing or preventing heart failure. (Mol Cell Biochem 263: 5-9, 2004).
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Koch WJdoi
10.1023/B:MCBI.0000041843.64809.48subject
Has Abstractpub_date
2004-08-01 00:00:00pages
5-9issue
1eissn
0300-8177issn
1573-4919pii
10.1023/B:MCBI.0000041843.64809.48journal_volume
263pub_type
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journal_title:Molecular and cellular biochemistry
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更新日期:2004-08-01 00:00:00
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