In 2019, around 17.9 million people died from cardiovascular disease, representing 32% of all global deaths. Identifying those at the highest risk of heart disease is crucial to ensure they receive appropriate treatment and prevent premature deaths.
Rhythm Through the Chambers
The heart has four chambers: two atria on the top and two ventricles on the bottom. The ability of the ventricles to pump oxygen-poor blood to the lungs and oxygen-rich blood to the other parts of the body depends on the atria, which refill the ventricles with blood consistently.
The atria are also a leading site for the disease known as atrial fibrillation. This condition occurs when these chambers no longer contract normally and carry out fast, uncoordinated, irregular heartbeats or arrhythmia. These chaotic beats damage the normal filling of the ventricles and could lead to stroke and heart failure.
Health experts have taken good tools to look at the atria to recognize the importance of relaxation properties to the heart's overall function. If the atria cannot do their job thoroughly, the ventricles cannot do theirs either.
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New Biomarker for Heart Disease
At Northwestern University, experts led by Professor Elizabeth McNally have discovered protein interactions in the atrium that play a vital role in normal heart function. The result of their study is discussed in the paper "Myosin-binding protein H-like regulates myosin-binding protein distribution and function in atrial cardiomyocytes."
The exact mechanisms that regulate atrial contraction and relaxation have garnered interest with the discovery of previously unappreciated proteins. In a previous study, scientists discovered the MYBP-HL gene, whose mutations increase the risk of arrhythmia and cardiomyopathy.
MYBP-HL is a gene that encodes myosin-binding protein H-like, which composes the contractile machinery in the atria. It also belongs to the same protein family as myosin-binding protein-C (cMyBP-C), which functions as a braking system for the heart to prevent it from over-contracting.
Mutations in the gene encoding cMyBP-C are a crucial cause of hypertrophic cardiomyopathy. However, the interaction between these two proteins and their impact on ventricle and atria function remains poorly understood.
In the current study, the researchers use immuno-electron, structured illumination, and mass spectroscopy to analyze heart cells from genetic mouse models. The research team identified a new binding relationship between MyBP-HL and cMyBP-C from these testing methods.
It was found that the loss of MyBP-HL doubled the amount of cMyBP-C in the atria, while the loss of cMyBP-C doubled the amount of MyBP-HL in the atria. Additionally, the loss of MyBP-HL accelerated atrial relaxation. The findings reveal a novel mechanism and essential role for MyBP-HL in regulating atrial relaxation and function.
The findings also shed light on the abnormal atrial relaxation properties observed in heart failure and the heart as it ages. Since the atria become stiffer with age, MyBP-HL could be a biomarker for atrial abnormalities like atrial fibrillation. According to study first author Dave Barefield, the findings provide a new potential therapeutic target to modulate atrial contractile function.
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