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Related Concept Videos

Conduction System of the Heart01:20

Conduction System of the Heart

The cardiac conduction system produces and transmits electrical impulses that prompt myocardial contraction, ensuring efficient heart function. This intricate system ensures that the heart beats in a coordinated and efficient manner, beginning with the atria and then the ventricles. The conduction system optimizes cardiac output by maintaining this precise sequence, which is crucial for adequate blood circulation.
This system relies on the unique properties of nodal and Purkinje cells:...
Conduction System of the Heart01:19

Conduction System of the Heart

Autorhythmicity is a term that refers to the heart's inherent ability to generate electrical signals and instigate muscle contractions. This self-regulating conduction system within the heart consists of two key components: the pacemaker cells and specialized conducting cells.
The pacemaker cells are located in two primary nodes: the sinoatrial (SA) node and the atrioventricular (AV) node. The SA node pacemaker cells can autonomously depolarize, triggering an action potential that leads to the...
Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

The normal cardiac rhythm is a synchronized electrical activity that facilitates the regular and coordinated contraction of the heart muscle. This process is essential for efficient blood circulation throughout the body. The fundamental elements involved in establishing and maintaining this rhythm include the unique electrical properties of cardiac muscle cells, the sinoatrial (SA) node's pacemaker function, the specialized conducting system, and the ionic mechanisms underlying each phase of...
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
The Cardiac Cycle01:13

The Cardiac Cycle

The heart beats rhythmically in a sequence called the cardiac cycle—a rapid coordination of contraction (systole) and relaxation (diastole).
The Process
Electrical signals—sent from the sinoatrial (SA) node in the right atrial wall to the atrioventricular (AV) node between the right atrium and right ventricle—cause both atria to simultaneously contract. When the signal reaches the AV node, it pauses for approximately a tenth of a second, allowing the atria to contract and empty blood into the...
Regulation of Heart Rates01:31

Regulation of Heart Rates

The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...

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Related Experiment Video

Updated: Jul 15, 2026

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
08:52

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection

Published on: February 17, 2015

Tbx3 controls the sinoatrial node gene program and imposes pacemaker function on the atria.

Willem M H Hoogaars1, Angela Engel, Janynke F Brons

  • 1Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.

Genes & Development
|May 3, 2007
PubMed
Summary

Tbx3 is crucial for forming the heart's pacemaker (sinoatrial node). Its deficiency causes atrial cells to invade the node, leading to arrhythmias and ectopic pacemakers.

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice
09:32

Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice

Published on: October 23, 2016

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Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
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Published on: February 17, 2015

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice
09:32

Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice

Published on: October 23, 2016

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Molecular Cardiology

Background:

  • The sinoatrial node acts as the heart's pacemaker, regulating heart rate and rhythm.
  • Mechanisms governing sinoatrial node formation and specification remain largely unknown.
  • Tbx3, a transcriptional repressor, is expressed in the developing cardiac conduction system.

Purpose of the Study:

  • To elucidate the role of Tbx3 in sinoatrial node development and function.
  • To investigate how Tbx3 influences gene expression programs in cardiac precursor cells.
  • To determine the impact of Tbx3 deficiency and ectopic expression on heart rhythm.

Main Methods:

  • Analysis of Tbx3 expression patterns in developing cardiac tissue.
  • Lineage tracing to track Tbx3-positive and Tbx3-negative cell populations.
  • Gene expression profiling to compare sinoatrial node and atrial cells.
  • Studies using Tbx3-deficient and Tbx3-ectopically expressing mouse models.

Main Results:

  • Tbx3 expression demarcates the sinoatrial node region, distinct from surrounding atrial cells.
  • Lineage segregation occurs early, separating Tbx3-positive sinoatrial node precursors from Tbx3-negative atrial precursors.
  • Tbx3 deficiency leads to atrial gene program expansion into the sinoatrial node domain and loss of pacemaker gene expression.
  • Ectopic Tbx3 expression represses atrial phenotype and imposes pacemaker characteristics, causing arrhythmias and ectopic pacemakers.

Conclusions:

  • Tbx3 is essential for the specification and formation of the sinoatrial node.
  • Tbx3 acts as a key regulator of the pacemaker gene expression program and phenotype.
  • Dysregulation of Tbx3 contributes to cardiac arrhythmias by disrupting sinoatrial node development.