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.
authors.affiliation: Institute of Molecular Pathology, A-1030 Vienna, Austria.
authors.forename: Romeo
authors.initials: R
authors.lastname: Ricci
authors.forename: Urs
authors.initials: U
authors.lastname: Eriksson
authors.forename: Gavin Y
authors.initials: GY
authors.lastname: Oudit
authors.forename: Robert
authors.initials: R
authors.lastname: Eferl
authors.forename: Alexander
authors.initials: A
authors.lastname: Akhmedov
authors.forename: Izabela
authors.initials: I
authors.lastname: Sumara
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Sumara
authors.forename: Zamaneh
authors.initials: Z
authors.lastname: Kassiri
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: David
authors.forename: Latifa
authors.initials: L
authors.lastname: Bakiri
authors.forename: Bernd
authors.initials: B
authors.lastname: Sasse
authors.forename: Maria-Helena
authors.initials: MH
authors.lastname: Idarraga
authors.forename: Martina
authors.initials: M
authors.lastname: Rath
authors.forename: David
authors.initials: D
authors.lastname: Kurz
authors.forename: Hans-Christian
authors.initials: HC
authors.lastname: Theussl
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Perriard
authors.forename: Peter
authors.initials: P
authors.lastname: Backx
authors.forename: Josef M
authors.initials: JM
authors.lastname: Penninger
authors.forename: Erwin F
authors.initials: EF
authors.lastname: Wagner
mesh_terms: D000818:Animals; D002311:Cardiomyopathy, Dilated / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000378:metabolism*; D000099169:Fos-Related Antigen 1
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D000099169:Fos-Related Antigen 1