A recent study by scientists from The Ohio State University offers new hope for people suffering from certain heart rhythm disorders.
The researchers focused on a protein called calmodulin, vital in regulating our heartbeat, and the findings could open the door for innovative treatment strategies.
What Does Calmodulin Do?
Present in many body organs, including the heart, calmodulin is a protein responsible for managing the flow of charged sodium and calcium particles into and out of heart muscle cells.
This particle exchange keeps our heartbeats steady and rhythmic. Furthermore, calmodulin generates the electrical activity that is recorded during an electrocardiogram, a test that monitors heart electrical activity.
Calmodulinopathies: Dangerous Heart Rhythm Disorders
Scientists recently found that modifications in the calmodulin protein could result in severe heart rhythm disorders known as calmodulinopathies.
These disorders can be lethal, and effective treatments are currently lacking. The primary reason for this treatment shortage is our insufficient understanding of how these calmodulin changes cause arrhythmias.
The Ohio State University Study: A Breakthrough
The Ohio State University researchers closely investigated mutations in calmodulin. They discovered that a mutated form of calmodulin, termed D96V-CaM, contributes to arrhythmias.
This mutation enhances the flow of sodium ions in heart muscle cells, leading to an irregular release of calcium ions. Published in the Journal of Clinical Investigation, the team’s findings represent a significant advancement.
“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.
Promising Implications for Treatment
The implications of these findings could be profound for developing new treatments using existing drugs to manage this severe, currently incurable heart disorder.
To understand the implications of their findings, Radwanski and his team used a genetically engineered mouse model.
The study revealed that the mutated calmodulin D96V-CaM affects a specific sodium channel, NaV1.6, without impacting the most common sodium channel in heart muscle, NaV1.5.
The mutation induces heart arrhythmias by causing the abnormal release of calcium ions.
Radwanski is optimistic about the study’s implications.
“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 advantageous for patients with congenital and acquired arrhythmia syndromes.
The study was published in the Journal of Clinical Investigation.
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