Related Experiment Video

Updated: Apr 30, 2026

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
11:33

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

12.7K

The potential role of Kv4.3 K+ channel in heart hypertrophy

Rong Huo, Yue Sheng, Wen-Ting Guo

    Channels (Austin, Tex.)
    |April 26, 2014
    PubMed

    Insights

    Kv4.3 K+ channels are crucial for heart function. Their downregulation in heart failure affects action potential duration and can activate CaMKII, contributing to disease progression. Upregulation may offer protective benefits.

    Area of Science:

    • Cardiology
    • Molecular Biology
    • Electrophysiology

    Background:

    • Transient outward K+ current (I(to)) is vital for cardiac action potential repolarization.
    • Kv4.3 K+ channels are key components of I(to) and are implicated in heart diseases.
    • Reduced Kv4.3 K+ channel function is observed in cardiac hypertrophy and heart failure.

    Purpose of the Study:

    • To review changes in cardiac Kv4.3 K+ channels in heart diseases.
    • To discuss the role of Kv4.3 K+ channels in cardiac hypertrophy and heart failure.
    • To explore Kv4.3 K+ channel involvement independent of electrical function.

    Main Methods:

    • Literature review of studies on Kv4.3 K+ channels in cardiac conditions.
    • Analysis of experimental data from animal models (mice, rats) and human/canine studies.
    • Examination of molecular pathways involving calcium (Ca2+) and CaMKII.

    Main Results:

    • In rodents, Kv4.3 downregulation prolongs action potential duration (APD), increasing intracellular calcium and activating calcineurin.
    • In canines and humans, Kv4.3 channels have a less significant role in APD.
    • Downregulation of Kv4.3 channels can lead to CaMKII activation, promoting hypertrophy and heart failure.

    Conclusions:

    • Kv4.3 K+ channels play a role in heart hypertrophy/heart failure through both electrical and non-electrical pathways.
    • Non-electrical roles involve CaMKII dissociation and activation.
    • Modulating Kv4.3 K+ channels could be a therapeutic target, but requires careful consideration of potential benefits and harms via CaMKII.

    More Related Videos

    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique08:11

    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

    Published on: November 11, 2022

    3.1K
    Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples14:39

    Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

    Published on: April 21, 2014

    16.8K

    Related Concept Videos

    Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

    Cardiomyopathy III: Hypertrophic Cardiomyopathy

    Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
    805
    Heart Failure II: Pathophysiology01:29

    Heart Failure II: Pathophysiology

    Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
    1.9K
    G-Protein Gated Ion Channels01:21

    G-Protein Gated Ion Channels

    GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
    Sensory...
    5.5K
    Voltage-gated Ion Channels01:26

    Voltage-gated Ion Channels

    Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
    Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
    11.2K
    Cellular Adaptation II: Hypertrophy01:26

    Cellular Adaptation II: Hypertrophy

    Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy:...
    54
    Cardiac Action Potential01:30

    Cardiac Action Potential

    Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
    The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
    Ionic Basis of Cardiac Action Potentials
    11.8K