@article{Gilsbach_Schwaderer_Preissl-Disti_epige_progr-2018,
author = {Gilsbach, Ralf and Schwaderer, Martin and Preissl, 
          Sebastian and Grüning, Björn A. and Kranzhofer, David and 
          Schneider, Pedro and Nuhrenberg, Thomas G. and 
          Mulero-Navarro, Sonia and Weichenhan, Dieter and Braun, 
          Christian and Dressen, Martina and Jacobs, Adam R. and Lahm, 
          Harald and Doenst, Torsten and Backofen, Rolf and Krane, 
          Markus and Gelb, Bruce D. and Hein, Lutz},
title = {Distinct epigenetic programs regulate cardiac myocyte 
         development and disease in the human heart in vivo},
journal = {Nat Commun},
year = {2018},
doi = {10.1038/s41467-017-02762-z},
volume = {9},
user = {backofen},
pmid = {29374152},
pages = {391},
number = {1},
issn = {2041-1723},
abstract = {Epigenetic mechanisms and transcription factor networks 
            essential for differentiation of cardiac myocytes have been 
            uncovered. However, reshaping of the epigenome of these 
            terminally differentiated cells during fetal development, 
            postnatal maturation, and in disease remains unknown. Here, 
            we investigate the dynamics of the cardiac myocyte epigenome 
            during development and in chronic heart failure. We find 
            that prenatal development and postnatal maturation are 
            characterized by a cooperation of active CpG methylation and 
            histone marks at cis-regulatory and genic regions to shape 
            the cardiac myocyte transcriptome. In contrast, pathological 
            gene expression in terminal heart failure is accompanied by 
            changes in active histone marks without major alterations in 
            CpG methylation and repressive chromatin marks. Notably, 
            cis-regulatory regions in cardiac myocytes are significantly 
            enriched for cardiovascular disease-associated variants. 
            This study uncovers distinct layers of epigenetic regulation 
            not only during prenatal development and postnatal 
            maturation but also in diseased human cardiac myocytes.}
}