Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?

Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and...

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Veröffentlicht in:	Basic research in cardiology 2010-03, Vol.105 (2), p.219-226
Hauptverfasser:	Conraads, Viviane M., Vrints, Christiaan J., Rodrigus, Inez E., Hoymans, Vicky Y., Van Craenenbroeck, Emeline M., Bosmans, Johan, Claeys, Marc J., Van Herck, Paul, Linke, Axel, Schuler, Gerhard, Adams, Volker
Format:	Artikel
Sprache:	eng
Schlagworte:	Aged Biopsy Cardiology Coronary Artery Disease - metabolism Female Humans Male Medicine Medicine & Public Health Middle Aged Muscle Proteins - metabolism Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - pathology Original Contribution Proto-Oncogene Proteins c-akt - metabolism RNA, Messenger - metabolism Signal Transduction SKP Cullin F-Box Protein Ligases - metabolism Tripartite Motif Proteins Troponin I - metabolism Tumor Necrosis Factor-alpha - metabolism Ubiquitin-Protein Ligases - metabolism Ventricular Myosins - metabolism Ventricular Remodeling
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Zusammenfassung:	Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently (
ISSN:	0300-8428 1435-1803
DOI:	10.1007/s00395-009-0068-5