Distinct Functions of JunD in Cardiac Hypertrophy and Heart Failure

Overview

Journal Genes Dev

Specialty Molecular Biology

Date 2005 Jan 19

PMID 15655111

Citations 14

Authors

Romeo Ricci

Urs Eriksson

Gavin Y Oudit

Robert Eferl

Alexander Akhmedov

Izabela Sumara

Grzegorz Sumara

Zamaneh Kassiri

Jean-Pierre David

Latifa Bakiri

Bernd Sasse

Maria-Helena Idarraga

Martina Rath

David Kurz

Hans-Christian Theussl

Jean-Claude Perriard

Peter Backx

Josef M Penninger

Erwin F Wagner

Affiliations

Soon will be listed here.

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.

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