A new study by The Ohio State University brings hope to people suffering from certain heart rhythm disorders.
The team of scientists examined a protein called calmodulin, which plays a crucial role in regulating our heartbeat.
This research could pave the way for new treatment methods.
The Role of Calmodulin
Calmodulin is a protein present in many body organs, including the heart. In the heart, it manages the flow of charged sodium and calcium particles in and out of heart muscle cells.
This exchange of particles ensures our heartbeats remain steady and rhythmic.
Moreover, calmodulin also produces the electrical activity measured during an electrocardiogram, a test that checks your heart’s electrical activity.
Calmodulinopathies: A Heart Rhythm Disorder
In recent years, scientists discovered that changes in the calmodulin protein could lead to severe heart rhythm disorders, termed calmodulinopathies.
These disorders can be deadly, and unfortunately, we currently lack effective treatments. The primary reason for this lack of treatments is our limited understanding of how these changes in calmodulin result in arrhythmias.
New Findings on Calmodulin
The Ohio State University research team studied calmodulin mutations closely. They found that a mutated form of calmodulin, referred to as D96V-CaM, contributes to arrhythmias.
This mutation encourages the flow of sodium ions in heart muscle cells, leading to an irregular release of calcium ions.
The team’s findings, published in the Journal of Clinical Investigation, represent a significant breakthrough.
“We have discovered a new way calmodulin mutations affect sodium channels and lead to calmodulinopathy,” said principal investigator Przemysław Radwanski, an assistant professor at the Ohio State University College of Pharmacy.
Implications of the Study
These findings hold great promise for developing new treatments based on existing drugs. The treatment aims to manage this severe heart disorder that currently has no cure.
To understand the implications of their findings, Radwanski and his team used a genetically engineered mouse model.
The study found that the mutated calmodulin D96V-CaM affects a specific sodium channel, NaV1.6.
Interestingly, it does not impact the most common sodium channel in heart muscle, NaV1.5. The mutation promotes heart arrhythmias by causing the abnormal release of calcium ions.
Radwanski is hopeful about the implications of the study.
“By understanding how calmodulin-related heart diseases work, we aim to discover treatments that can prevent arrhythmias not only from calmodulin mutations but also from abnormal sodium-channel function,” he said.
This could be beneficial for patients with congenital and acquired arrhythmia syndromes.
If you care about heart health, please read studies about the best time to take vitamins to prevent heart disease, and scientists find how COVID-19 damages the heart.
For more information about heart health, please see recent studies about Aspirin linked to a higher risk of heart failure, and results showing this drug could reduce heart disease, fatty liver, and obesity.
The study was published in the Journal of Clinical Investigation.
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