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Related Experiment Video

Updated: Dec 15, 2025

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

Silencing miR-370-3p rescues funny current and sinus node function in heart failure.

Joseph Yanni¹, Alicia D'Souza¹, Yanwen Wang¹

¹Division of Cardiovascular Sciences, University of Manchester, 46 Grafton Street, Manchester, M13 9NT, UK.

Scientific Reports

|July 11, 2020

Summary

MicroRNA miR-370-3p causes bradycardia in heart failure by downregulating the HCN4 channel. Inhibiting miR-370-3p restores channel function, improves heart function, and reduces mortality in mice.

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

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

Published on: October 23, 2016

Area of Science:

Cardiology
Molecular Biology
Genetics

Background:

Bradyarrhythmias are a significant cause of mortality in heart failure.
Electrical remodeling of the HCN4 pacemaker channel is implicated in this process.

Purpose of the Study:

To investigate the role of microRNA miR-370-3p in heart failure-induced bradycardia.
To explore the therapeutic potential of targeting miR-370-3p for heart failure treatment.

Main Methods:

Utilized a mouse model of heart failure exhibiting sinus bradycardia.
Investigated the effects of miR-370-3p on HCN4 expression and function in vitro and in vivo.
Administered an antimiR to miR-370-3p in heart failure mice.

Main Results:

Heart failure mice showed increased miR-370-3p, decreased HCN4, and reduced I_f current.
Exogenous miR-370-3p inhibited HCN4 and caused bradycardia in isolated sinus nodes.
AntimiR treatment restored HCN4, I_f, blunted bradycardia, improved ventricular function, and reduced mortality.

Conclusions:

miR-370-3p plays a key role in heart failure-related bradycardia by targeting HCN4.
Inhibition of miR-370-3p offers a novel therapeutic strategy for heart failure.