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Digitale Medien

THE CARDIAC FIBROBLAST: Therapeutic Target in Myocardial Remodeling and Failure (2005)

Brown, R. Dale ; Ambler, S. Kelly ; Mitchell, M. Darren ; [weitere]

Palo Alto, Calif. : Annual Reviews

Annual Review of Pharmacology 45 (2005), S. 657-687

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ISSN: 0362-1642

Quelle: Annual Reviews Electronic Back Volume Collection 1932-2001ff

Thema: Medizin , Chemie und Pharmazie

Notizen: Cardiac fibroblasts play a central role in the maintenance of extracellular matrix in the normal heart and as mediators of inflammatory and fibrotic myocardial remodeling in the injured and failing heart. In this review, we evaluate the cardiac fibroblast as a therapeutic target in heart disease. Unique features of cardiac fibroblast cell biology are discussed in relation to normal and pathophysiological cardiac function. The contribution of cardiac fibrosis as an independent risk factor in the outcome of heart failure is considered. Candidate drug therapies that derive benefit from actions on cardiac fibroblasts are summarized, including inhibitors of angiotensin-aldosterone systems, endothelin receptor antagonists, statins, anticytokine therapies, matrix metalloproteinase inhibitors, and novel antifibrotic/anti-inflammatory agents. These findings point the way to future challenges in cardiac fibroblast biology and pharmacotherapy.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1146/annurev.pharmtox.45.120403.095802

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Digitale Medien

Adrenergic hormones and control of cardiac myocyte growth (1991)

Simpson, Paul ; Simpson, C. ; Kariya, Ken-ichi ; [weitere]

Springer

Molecular and cellular biochemistry 104 (1991), S. 35-43

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ISSN: 1573-4919

Schlagwort(e): α1-adrenergic receptors ; β-adrenergic receptors ; cardiac muscle ; cell culture ; gene expression ; protein kinase C

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie , Medizin

Notizen: Abstract The molecular mechanisms of cardiac myocyte growth are relevant to important problems in cardiovascular disease. A cell culture model has been developed to explore the role of adrenergic hormones in cardiac myocyte growth and gene expression. Activation of a cardiac myocyte α1-adrenergic receptor by catecholamines induces hypertrophic growth of neonatal rat cardiac myocytes and initiates selective increases in contractile protein gene transcription. These effects on growth and gene expression do not depend on contractile activity. The cardiac myocytes contain at least two subtypes of α1-adrenergic receptors and at least three isoforms of protein kinase C (PKC). A distinct α1 receptor subtype may mediate hypertrophy and gene transcription. Different isoforms of PKC are translocated to different intracellular sites on activation, and there is evidence that the β-PKC isoform may be an element in the signal transduction pathway from an α1 receptor at the surface to the cardiac myocyte nucleus. Growth regulation through a β-adrenergic receptor can also be demonstrated in the culture model. The growth response mediated through a β-adrenergic receptor differs in several respects from that transduced through an al adrenergic receptor.