Abstract

Since its discovery, myosin-binding protein C (cMyBP-C) has become a protein of interest clinically. With emergence of new methodologies and technologies, the structure and functions of cMyBP-C from different aspects can be studied, enabling us to better understand its involvement in certain cardiac conditions. Studying its kinetics of release and clearance from the circulation and by comparing to other conventional biomarkers, it has been reported that cMyBP-C is eligible to be a novel biomarker for several cardiac conditions. Moreover, studying the genetics and their involvement in pathogenic mechanisms has opened the ideas for potential therapeutic strategies. More and more researches are constantly being done to better understand the role of cMyBP-C in dilated cardiomyopathy (DCM). The importance of cMyBP-C to the heart is still actively being investigated. Its presence is however crucial for sarcomere organization and proper regulation of cardiac contraction during systole and complete relaxation during diastole. Genetic mutation in cMyBP-C has been linked to cardiac conditions including hypertrophic and dilated cardiomyopathies. Around 350 types of mutations have already been documented leading to various cardiac conditions and abnormalities. Analyzing human heart samples has enabled us to better understand the importance of cMyBP-C and how its mutations lead to inherited cardiomyopathies. It is therefore necessary to have an update about the research progress of cMyBP-C in relation to DCM and other cardiac conditions.

Highlights

  • Dilated cardiomyopathy (DCM) is the most common type of cardiomyopathies seen clinically

  • Its presence is crucial for sarcomere organization and proper regulation of cardiac contraction during systole and complete relaxation during diastole

  • Genetic mutation in cMyBP-C has been linked to cardiac conditions including hypertrophic and dilated cardiomyopathies

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Summary

Introduction

Dilated cardiomyopathy (DCM) is the most common type of cardiomyopathies seen clinically. DCM can be due to idiopathic causes, which is principally due to gene mutations in specific cardiac proteins [5] [6]. The main clinical manifestations of DCM patients are chest tightness, palpitation, dyspnea and decreased activity tolerance, serious symptoms of heart failure in more severe cases, and even appearance of serious heart arrhythmias. Current treatment methods are only to improve the symptoms of heart failure and to prevent complications. DCM mainly manifests as a declination of systolic and diastolic functions. There are a wide variety of structural cardiac proteins involved in myocardial contraction and relaxation. One protein of great interest is cMyBP-C. The latter is an important regulotory component of the sarcomere which ensures proper regulation of heart systolic and diastolic function. We emphasize on an update about the research progress of cMyBP-C and its relation to DCM and other cardiac conditions

Classification of cMyBP
Phosphorylation of cMyBP-C
Findings
Conclusion
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