Inhibition of protein kinase C reduces left ventricular fibrosis and dysfunction following myocardial infarction
| Autor: | Yuan Zhang, Darren J. Kelly, Andrew J. Boyle, Richard E. Gilbert, Silviu Itescu, Renae M. Gow, Kerrie Way, Henry Krum, Alison J. Cox |
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| Rok vydání: | 2004 |
| Předmět: |
Cardiac function curve
Male medicine.medical_specialty Indoles Heart Ventricles Myocardial Infarction Infarction Ruboxistaurin Pathogenesis Maleimides Rats Sprague-Dawley chemistry.chemical_compound Ventricular Dysfunction Left Fibrosis Transforming Growth Factor beta Internal medicine Medicine Animals Myocardial infarction Molecular Biology In Situ Hybridization Protein Kinase C business.industry medicine.disease Extracellular Matrix Rats chemistry Gene Expression Regulation Echocardiography Heart failure Cardiology Myocardial infarction complications Collagen Cardiology and Cardiovascular Medicine business |
| Zdroj: | Journal of molecular and cellular cardiology. 39(2) |
| ISSN: | 0022-2828 |
| Popis: | Despite current therapies, chronic heart failure (CHF) remains a major complication of myocardial infarction (MI). The pathological changes that follow MI extend to regions remote from the site of infarction (non-infarct zone, NIZ) where fibrosis is a prominent finding. Although the mechanisms underlying this adverse remodeling are incompletely understood, activation of protein kinase C has recently been implicated in its pathogenesis. MI was induced in Sprague-Dawley rats by ligation of the left anterior descending coronary artery. One week post-MI, animals were randomized to receive the PKC-inhibitor, ruboxistaurin (LY333531) for 4 weeks, or no treatment. When compared with sham-operated animals, post-MI rats showed a 33+/-7% reduction in fractional shortening over a 4 weeks period, that was attenuated by treatment with ruboxistaurin (6+/-11%, P |
| Databáze: | OpenAIRE |
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