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Published on: June 14, 2016
Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies
Jarmila Machackova1, Judit Barta, Naranjan S Dhalla
1Institute of Cardiovascular Sciences, St Boniface General Hospital Research Center, Depatment of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Insights
Cardiac remodeling and heart failure involve changes in heart muscle proteins. Myofibrillar remodeling, affecting contractile and regulatory proteins, is linked to cardiac dysfunction in heart disease.
Area of Science:
- Cardiovascular Research
- Molecular Cardiology
- Biochemistry
Background:
- Pathological conditions frequently cause cardiac remodeling and myocardial dysfunction.
- Mechanisms underlying the transition from adaptive to maladaptive cardiac changes and heart failure development remain unclear.
Purpose of the Study:
- This review focuses on myofibrillar remodeling in hypertrophied and failing myocardium across various heart diseases.
- It aims to identify molecular and biochemical alterations in myofibrils, contractile proteins, and regulatory proteins.
Main Methods:
- Review of extensive studies on subcellular structures, signal transduction, and metabolism in cardiovascular disorders.
- Analysis of reported changes in gene expression for contractile and regulatory proteins.
- Examination of myofibrillar remodeling resulting from proteolysis, oxidation, and phosphorylation.
Main Results:
- Gene expression changes in contractile and regulatory proteins are observed in failing hearts and heart diseases.
- These alterations may precede heart failure, cardiac hypertrophy, and cardiomyopathies.
- Myofibrillar remodeling, involving protein modifications, is described in failing hearts of diverse etiologies.
Conclusions:
- Myofibrillar remodeling is associated with cardiac dysfunction.
- Alterations in contractile and regulatory proteins are contingent upon the specific heart disease type and its progression stage.
Background:
A wide variety of pathological conditions have been shown to result in cardiac remodelling and myocardial dysfunction. However, the mechanisms of transition from adaptive to maladaptive alterations, as well as those for changes in cardiac performance leading to heart failure, are poorly understood.
Observations:
Extensive studies have revealed a broad spectrum of progressive changes in subcellular structures and function, as well as in signal transduction and metabolism in the heart, among different cardiovascular disorders. The present review is focused on identifying the alterations in molecular and biochemical structure of myofibrils (myofibrillar remodelling) in hypertrophied and failing myocardium in different types of heart diseases. Numerous changes at the level of gene expression for both contractile and regulatory proteins have already been reported in failing hearts and heart diseases; these changes are potential precursors for heart failure such as cardiac hypertrophy and cardiomyopathies. Myofibrillar remodelling, as a consequence of proteolysis, oxidation, and phosphorylation of some functional groups in both contractile and regulatory proteins in hearts failing due to different etiologies, has also been described.
Conclusions:
Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractile and regulatory proteins are dependent on the type and stage of heart disease.
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