The molecular and functional identities of atrial cardiomyocytes in health and disease

Sören Brandenburg; Eric C Arakel; Blanche Schwappach; Stephan E Lehnart

doi:10.1016/j.bbamcr.2015.11.025

The molecular and functional identities of atrial cardiomyocytes in health and disease

Standard

The molecular and functional identities of atrial cardiomyocytes in health and disease. / Brandenburg, Sören; Arakel, Eric C; Schwappach, Blanche; Lehnart, Stephan E.

In: Biochim Biophys Acta, Vol. 1863, No. 7 Pt B, 07.2016, p. 1882-93.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Brandenburg, S, Arakel, EC, Schwappach, B & Lehnart, SE 2016, 'The molecular and functional identities of atrial cardiomyocytes in health and disease', Biochim Biophys Acta, vol. 1863, no. 7 Pt B, pp. 1882-93. https://doi.org/10.1016/j.bbamcr.2015.11.025

APA

Brandenburg, S., Arakel, E. C., Schwappach, B., & Lehnart, S. E. (2016). The molecular and functional identities of atrial cardiomyocytes in health and disease. Biochim Biophys Acta, 1863(7 Pt B), 1882-93. https://doi.org/10.1016/j.bbamcr.2015.11.025

Vancouver

Brandenburg S, Arakel EC, Schwappach B, Lehnart SE. The molecular and functional identities of atrial cardiomyocytes in health and disease. Biochim Biophys Acta. 2016 Jul;1863(7 Pt B):1882-93. https://doi.org/10.1016/j.bbamcr.2015.11.025

Bibtex

@article{9d882fa93eb84cb3b5ff22f9599a5f7f,

title = "The molecular and functional identities of atrial cardiomyocytes in health and disease",

abstract = "Atrial cardiomyocytes are essential for fluid homeostasis, ventricular filling, and survival, yet their cell biology and physiology are incompletely understood. It has become clear that the cell fate of atrial cardiomyocytes depends significantly on transcription programs that might control thousands of differentially expressed genes. Atrial muscle membranes propagate action potentials and activate myofilament force generation, producing overall faster contractions than ventricular muscles. While atria-specific excitation and contractility depend critically on intracellular Ca(2+) signalling, voltage-dependent L-type Ca(2+) channels and ryanodine receptor Ca(2+) release channels are each expressed at high levels similar to ventricles. However, intracellular Ca(2+) transients in atrial cardiomyocytes are markedly heterogeneous and fundamentally different from ventricular cardiomyocytes. In addition, differential atria-specific K(+) channel expression and trafficking confer unique electrophysiological and metabolic properties. Because diseased atria have the propensity to perpetuate fast arrhythmias, we discuss our understanding about the cell-specific mechanisms that lead to metabolic and/or mitochondrial dysfunction in atrial fibrillation. Interestingly, recent work identified potential atria-specific mechanisms that lead to early contractile dysfunction and metabolic remodelling, suggesting highly interdependent metabolic, electrical, and contractile pathomechanisms. Hence, the objective of this review is to provide an integrated model of atrial cardiomyocytes, from tissue-specific cell properties, intracellular metabolism, and excitation-contraction (EC) coupling to early pathological changes, in particular metabolic dysfunction and tissue remodelling due to atrial fibrillation and aging. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel. ",

keywords = "Action Potentials, Animals, Atrial Fibrillation/genetics, Atrial Function, Atrial Remodeling, Calcium Signaling, Cell Differentiation, Cell Lineage, Heart Atria/metabolism, Humans, Myocardial Contraction, Myocytes, Cardiac/metabolism, Phenotype",

author = "S{\"o}ren Brandenburg and Arakel, {Eric C} and Blanche Schwappach and Lehnart, {Stephan E}",

note = "Copyright {\textcopyright} 2015. Published by Elsevier B.V.",

year = "2016",

month = jul,

doi = "10.1016/j.bbamcr.2015.11.025",

language = "English",

volume = "1863",

pages = "1882--93",

journal = "Biochim Biophys Acta",

issn = "0006-3002",

number = "7 Pt B",

}

RIS

TY - JOUR

T1 - The molecular and functional identities of atrial cardiomyocytes in health and disease

AU - Brandenburg, Sören

AU - Arakel, Eric C

AU - Schwappach, Blanche

AU - Lehnart, Stephan E

PY - 2016/7

Y1 - 2016/7

N2 - Atrial cardiomyocytes are essential for fluid homeostasis, ventricular filling, and survival, yet their cell biology and physiology are incompletely understood. It has become clear that the cell fate of atrial cardiomyocytes depends significantly on transcription programs that might control thousands of differentially expressed genes. Atrial muscle membranes propagate action potentials and activate myofilament force generation, producing overall faster contractions than ventricular muscles. While atria-specific excitation and contractility depend critically on intracellular Ca(2+) signalling, voltage-dependent L-type Ca(2+) channels and ryanodine receptor Ca(2+) release channels are each expressed at high levels similar to ventricles. However, intracellular Ca(2+) transients in atrial cardiomyocytes are markedly heterogeneous and fundamentally different from ventricular cardiomyocytes. In addition, differential atria-specific K(+) channel expression and trafficking confer unique electrophysiological and metabolic properties. Because diseased atria have the propensity to perpetuate fast arrhythmias, we discuss our understanding about the cell-specific mechanisms that lead to metabolic and/or mitochondrial dysfunction in atrial fibrillation. Interestingly, recent work identified potential atria-specific mechanisms that lead to early contractile dysfunction and metabolic remodelling, suggesting highly interdependent metabolic, electrical, and contractile pathomechanisms. Hence, the objective of this review is to provide an integrated model of atrial cardiomyocytes, from tissue-specific cell properties, intracellular metabolism, and excitation-contraction (EC) coupling to early pathological changes, in particular metabolic dysfunction and tissue remodelling due to atrial fibrillation and aging. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.

AB - Atrial cardiomyocytes are essential for fluid homeostasis, ventricular filling, and survival, yet their cell biology and physiology are incompletely understood. It has become clear that the cell fate of atrial cardiomyocytes depends significantly on transcription programs that might control thousands of differentially expressed genes. Atrial muscle membranes propagate action potentials and activate myofilament force generation, producing overall faster contractions than ventricular muscles. While atria-specific excitation and contractility depend critically on intracellular Ca(2+) signalling, voltage-dependent L-type Ca(2+) channels and ryanodine receptor Ca(2+) release channels are each expressed at high levels similar to ventricles. However, intracellular Ca(2+) transients in atrial cardiomyocytes are markedly heterogeneous and fundamentally different from ventricular cardiomyocytes. In addition, differential atria-specific K(+) channel expression and trafficking confer unique electrophysiological and metabolic properties. Because diseased atria have the propensity to perpetuate fast arrhythmias, we discuss our understanding about the cell-specific mechanisms that lead to metabolic and/or mitochondrial dysfunction in atrial fibrillation. Interestingly, recent work identified potential atria-specific mechanisms that lead to early contractile dysfunction and metabolic remodelling, suggesting highly interdependent metabolic, electrical, and contractile pathomechanisms. Hence, the objective of this review is to provide an integrated model of atrial cardiomyocytes, from tissue-specific cell properties, intracellular metabolism, and excitation-contraction (EC) coupling to early pathological changes, in particular metabolic dysfunction and tissue remodelling due to atrial fibrillation and aging. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.

KW - Action Potentials

KW - Animals

KW - Atrial Fibrillation/genetics

KW - Atrial Function

KW - Atrial Remodeling

KW - Calcium Signaling

KW - Cell Differentiation

KW - Cell Lineage

KW - Heart Atria/metabolism

KW - Humans

KW - Myocardial Contraction

KW - Myocytes, Cardiac/metabolism

KW - Phenotype

U2 - 10.1016/j.bbamcr.2015.11.025

DO - 10.1016/j.bbamcr.2015.11.025

M3 - SCORING: Review article

C2 - 26620800

VL - 1863

SP - 1882

EP - 1893

JO - Biochim Biophys Acta

JF - Biochim Biophys Acta

SN - 0006-3002

IS - 7 Pt B

ER -