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Distinct functions of junD in cardiac hypertrophy and heart failure

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Distinct functions of junD in cardiac hypertrophy and heart failure. / Ricci, Romeo; Eriksson, Urs; Oudit, Gavin Y; Eferl, Robert; Akhmedov, Alexander; Sumara, Izabela; Sumara, Grzegorz; Kassiri, Zamaneh; David, Jean-Pierre; Bakiri, Latifa; Sasse, Bernd; Idarraga, Maria-Helena; Rath, Martina; Kurz, David; Theussl, Hans-Christian; Perriard, Jean-Claude; Backx, Peter; Penninger, Josef M; Wagner, Erwin F.

In: GENE DEV, Vol. 19, No. 2, 15.01.2005, p. 208-13.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ricci, R, Eriksson, U, Oudit, GY, Eferl, R, Akhmedov, A, Sumara, I, Sumara, G, Kassiri, Z, David, J-P, Bakiri, L, Sasse, B, Idarraga, M-H, Rath, M, Kurz, D, Theussl, H-C, Perriard, J-C, Backx, P, Penninger, JM & Wagner, EF 2005, 'Distinct functions of junD in cardiac hypertrophy and heart failure', GENE DEV, vol. 19, no. 2, pp. 208-13. https://doi.org/10.1101/gad.327005

APA

Ricci, R., Eriksson, U., Oudit, G. Y., Eferl, R., Akhmedov, A., Sumara, I., Sumara, G., Kassiri, Z., David, J-P., Bakiri, L., Sasse, B., Idarraga, M-H., Rath, M., Kurz, D., Theussl, H-C., Perriard, J-C., Backx, P., Penninger, J. M., & Wagner, E. F. (2005). Distinct functions of junD in cardiac hypertrophy and heart failure. GENE DEV, 19(2), 208-13. https://doi.org/10.1101/gad.327005

Vancouver

Ricci R, Eriksson U, Oudit GY, Eferl R, Akhmedov A, Sumara I et al. Distinct functions of junD in cardiac hypertrophy and heart failure. GENE DEV. 2005 Jan 15;19(2):208-13. https://doi.org/10.1101/gad.327005

Bibtex

@article{aaa6d43ab422400d8f0b3fa83e3d51b4,
title = "Distinct functions of junD in cardiac hypertrophy and heart failure",
abstract = "Cardiac hypertrophic stimuli induce both adaptive and maladaptive growth response pathways in heart. Here we show that mice lacking junD develop less adaptive hypertrophy in heart after mechanical pressure overload, while cardiomyocyte-specific expression of junD in mice results in spontaneous ventricular dilation and decreased contractility. In contrast, fra-1 conditional knock-out mice have a normal hypertrophic response, whereas hearts from fra-1 transgenic mice decompensate prematurely. Moreover, fra-1 transgenic mice simultaneously lacking junD reveal a spontaneous dilated cardiomyopathy associated with increased cardiomyocyte apoptosis and a primary mitochondrial defect. These data suggest that junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels.",
keywords = "Animals, Cardiomyopathy, Dilated, Gene Expression Regulation, Heart Failure, Mice, Mice, Knockout, Myocardium, Myocytes, Cardiac, Proto-Oncogene Proteins c-fos, Proto-Oncogene Proteins c-jun",
author = "Romeo Ricci and Urs Eriksson and Oudit, {Gavin Y} and Robert Eferl and Alexander Akhmedov and Izabela Sumara and Grzegorz Sumara and Zamaneh Kassiri and Jean-Pierre David and Latifa Bakiri and Bernd Sasse and Maria-Helena Idarraga and Martina Rath and David Kurz and Hans-Christian Theussl and Jean-Claude Perriard and Peter Backx and Penninger, {Josef M} and Wagner, {Erwin F}",
year = "2005",
month = jan,
day = "15",
doi = "10.1101/gad.327005",
language = "English",
volume = "19",
pages = "208--13",
journal = "GENE DEV",
issn = "0890-9369",
publisher = "Cold Spring Harbor Laboratory Press",
number = "2",

}

RIS

TY - JOUR

T1 - Distinct functions of junD in cardiac hypertrophy and heart failure

AU - Ricci, Romeo

AU - Eriksson, Urs

AU - Oudit, Gavin Y

AU - Eferl, Robert

AU - Akhmedov, Alexander

AU - Sumara, Izabela

AU - Sumara, Grzegorz

AU - Kassiri, Zamaneh

AU - David, Jean-Pierre

AU - Bakiri, Latifa

AU - Sasse, Bernd

AU - Idarraga, Maria-Helena

AU - Rath, Martina

AU - Kurz, David

AU - Theussl, Hans-Christian

AU - Perriard, Jean-Claude

AU - Backx, Peter

AU - Penninger, Josef M

AU - Wagner, Erwin F

PY - 2005/1/15

Y1 - 2005/1/15

N2 - Cardiac hypertrophic stimuli induce both adaptive and maladaptive growth response pathways in heart. Here we show that mice lacking junD develop less adaptive hypertrophy in heart after mechanical pressure overload, while cardiomyocyte-specific expression of junD in mice results in spontaneous ventricular dilation and decreased contractility. In contrast, fra-1 conditional knock-out mice have a normal hypertrophic response, whereas hearts from fra-1 transgenic mice decompensate prematurely. Moreover, fra-1 transgenic mice simultaneously lacking junD reveal a spontaneous dilated cardiomyopathy associated with increased cardiomyocyte apoptosis and a primary mitochondrial defect. These data suggest that junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels.

AB - Cardiac hypertrophic stimuli induce both adaptive and maladaptive growth response pathways in heart. Here we show that mice lacking junD develop less adaptive hypertrophy in heart after mechanical pressure overload, while cardiomyocyte-specific expression of junD in mice results in spontaneous ventricular dilation and decreased contractility. In contrast, fra-1 conditional knock-out mice have a normal hypertrophic response, whereas hearts from fra-1 transgenic mice decompensate prematurely. Moreover, fra-1 transgenic mice simultaneously lacking junD reveal a spontaneous dilated cardiomyopathy associated with increased cardiomyocyte apoptosis and a primary mitochondrial defect. These data suggest that junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels.

KW - Animals

KW - Cardiomyopathy, Dilated

KW - Gene Expression Regulation

KW - Heart Failure

KW - Mice

KW - Mice, Knockout

KW - Myocardium

KW - Myocytes, Cardiac

KW - Proto-Oncogene Proteins c-fos

KW - Proto-Oncogene Proteins c-jun

U2 - 10.1101/gad.327005

DO - 10.1101/gad.327005

M3 - SCORING: Journal article

C2 - 15655111

VL - 19

SP - 208

EP - 213

JO - GENE DEV

JF - GENE DEV

SN - 0890-9369

IS - 2

ER -