Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

USP7 inhibition perturbs proteostasis and tumorigenesis in triple-negative breast cancer.

NPJ breast cancer·2026

Same author

DDX3X-mediated translation of structured cardiac mRNAs is essential for female heart development.

Genes & development·2026

Same author

PCBP1 regulates alternative splicing of AARS2 in congenital cardiomyopathy.

Nature cardiovascular research·2026

Same author

TBX5 and CHD4 Coordinately Activate Atrial Cardiomyocyte Genes to Maintain Cardiac Rhythm Homeostasis.

Circulation·2025

Same author

ERK signaling promotes IKKε expression and oncogenic functions in pancreatic cancer cells in association with TBK1.

The Journal of biological chemistry·2025

Same author

Metaproteomics-based stable isotope fingerprinting links intestinal bacteria to their carbon source and captures diet-induced substrate switching.

The ISME journal·2025

Search research articles

Related Experiment Video

Updated: May 19, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Published on: June 14, 2020

Biomechanical Isolation is Required for Maintenance of the Cardiac Pacemaker Cell Fate.

Michael Bressan¹, Ashlyn Laidman², Trevor Henley²

¹University of North Carolina at Chapel Hill.

Research Square

|May 18, 2026

Summary

Cardiac pacemaker cells (CPCs) require mechanical uncoupling to maintain heart rhythm. Suppressing mechanotransduction prevents electrical dysfunction, revealing a new regulatory mechanism for cardiac pacemaking.

More Related Videos

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

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

Published on: February 17, 2015

Isolation of High Quality Murine Atrial and Ventricular Myocytes for Simultaneous Measurements of Ca2+ Transients and L-Type Calcium Current

Isolation of High Quality Murine Atrial and Ventricular Myocytes for Simultaneous Measurements of Ca²⁺ Transients and L-Type Calcium Current

Published on: November 3, 2020

Related Experiment Videos

Last Updated: May 19, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Published on: June 14, 2020

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

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

Published on: February 17, 2015

Isolation of High Quality Murine Atrial and Ventricular Myocytes for Simultaneous Measurements of Ca2+ Transients and L-Type Calcium Current

Isolation of High Quality Murine Atrial and Ventricular Myocytes for Simultaneous Measurements of Ca²⁺ Transients and L-Type Calcium Current

Published on: November 3, 2020

Area of Science:

Cardiology
Molecular Biology
Cellular Physiology

Background:

The sinoatrial node (SAN) generates electrical impulses for heart rhythm via cardiac pacemaker cells (CPCs).
The upstream cellular events regulating SAN electrophysiology are not fully understood.
Ionic mechanisms of CPC function are well-studied, but mechanical signaling's role is unclear.

Purpose of the Study:

To investigate the role of mechanical signaling in cardiac pacemaker cell function.
To identify molecular mechanisms underlying SAN electrophysiological properties.
To understand how cellular strain affects CPCs.

Main Methods:

Quantitative proteomic analysis of developing CPCs.
Investigating the effects of ectopic mechanotransduction pathway activation in CPCs.
Assessing the impact of cellular strain on ion channels and transcription factors in CPCs.

Main Results:

Developing CPCs lack machinery for sensing mechanical cues.
Activating mechanotransduction pathways in CPCs causes SAN electrical dysfunction.
Cellular strain downregulates ion channels and transcription factors essential for CPC function.

Conclusions:

Mechanical uncoupling is critical for cardiac pacemaking.
Suppression of mechanotransductive signaling pathways is a key regulatory mechanism for SAN function.
This study uncovers a novel regulatory mechanism essential for maintaining cardiac rhythm.