Scientists Discover How Gene Interactions In Atrium Contribute To Cardiovascular Disease Risk

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In the year 2019, approximately 17.9 million individuals succumbed to cardiovascular ailments, constituting 32% of worldwide fatalities. Recognizing individuals with heightened susceptibility to heart disease is vital for administering suitable interventions, thereby averting untimely mortality and ensuring optimal healthcare outcomes.

Atrial fibrillation causes irregular heartbeats

In the intricate orchestration of the heart’s functions, its four chambers play a vital role. Positioned as pairs – two atria above and two ventricles below – they collaborate to ensure the efficient circulation of oxygen-poor and oxygen-rich blood. However, atrial fibrillation, a disorder affecting the atria, disrupts this harmony, causing irregular heartbeats.

Health professionals have employed effective methodologies to examine the atria, emphasizing the significance of relaxation properties in contributing to the overall functionality of the heart. If the atria are unable to perform their duties adequately, the ventricles are also hindered in carrying out their respective functions.

In a recent groundbreaking research conducted at Northwestern University, Professor Elizabeth McNally and her team have identified novel protein interactions within the atrium that are crucial for maintaining normal heart function. The findings of their investigation are detailed in the scientific paper titled “Regulation of Myosin-binding Protein Distribution and Function in Atrial Cardiomyocytes by Myosin-binding Protein H-like.”

MYBP-HL gene variation elevate risk of cardiomyopathy and arrhythmia

The exploration of the intricate mechanisms governing atrial contraction and relaxation has attracted significant attention due to the revelation of previously overlooked proteins. A prior study unearthed the MYBP-HL gene, and its genetic variations were found to elevate the susceptibility to arrhythmia and cardiomyopathy.

MYBP-HL encodes myosin-binding protein H-like, a component of atrial contractile machinery, sharing a protein family with myosin-binding protein-C (cMyBP-C), a heart braking system. Mutations in cMyBP-C gene cause hypertrophic cardiomyopathy. Investigating heart cells from genetic mouse models using immuno-electron, structured illumination, and mass spectroscopy, researchers revealed a novel binding relationship between MyBP-HL and cMyBP-C.

The study revealed that the absence of MyBP-HL resulted in a twofold increase in cMyBP-C levels in the atria, whereas the absence of cMyBP-C led to a twofold increase in MyBP-HL levels. Furthermore, the absence of MyBP-HL expedited atrial relaxation, highlighting its crucial role.

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