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Circ Res. 2017 Sep 29;121(8):1000-1020. doi: 10.1161/CIRCRESAHA.117.310355.

Calcium Signaling and Transcriptional Regulation in Cardiomyocytes.

Author information

1
From the Department of Molecular Cardiology and Epigenetics (M.D., A.v.d.L., J.B.) and Department of Cardiology (H.A.K.), Heidelberg University, Germany; and DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Germany (M.D., A.v.d.L., H.A.K., J.B.).
2
From the Department of Molecular Cardiology and Epigenetics (M.D., A.v.d.L., J.B.) and Department of Cardiology (H.A.K.), Heidelberg University, Germany; and DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Germany (M.D., A.v.d.L., H.A.K., J.B.). Johannes.backs@med.uni-heidelberg.de.

Abstract

Calcium (Ca2+) is a universal regulator of various cellular functions. In cardiomyocytes, Ca2+ is the central element of excitation-contraction coupling, but also impacts diverse signaling cascades and influences the regulation of gene expression, referred to as excitation-transcription coupling. Disturbances in cellular Ca2+-handling and alterations in Ca2+-dependent gene expression patterns are pivotal characteristics of failing cardiomyocytes, with several excitation-transcription coupling pathways shown to be critically involved in structural and functional remodeling processes. Thus, targeting Ca2+-dependent transcriptional pathways might offer broad therapeutic potential. In this article, we (1) review cytosolic and nuclear Ca2+ dynamics in cardiomyocytes with respect to their impact on Ca2+-dependent signaling, (2) give an overview on Ca2+-dependent transcriptional pathways in cardiomyocytes, and (3) discuss implications of excitation-transcription coupling in the diseased heart.

KEYWORDS:

calcineurin; calcium; calcium-calmodulin dependent protein kinase II; calmodulin; excitation transcription coupling

PMID:
28963192
DOI:
10.1161/CIRCRESAHA.117.310355
[Indexed for MEDLINE]

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