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Novel Mechanistic Roles for Ankyrin-G in Cardiac Remodeling and Heart Failure
Michael A Makara1,2, Jerry Curran1,2, Ellen R Lubbers1,2
1Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University Wexner Medical Center and College of Medicine, Columbus, Ohio.
JACC. Basic to Translational Science
|November 21, 2018
Summary
Ankyrin-G is vital for heart adaptation to stress and aging. Disruption of this protein contributes to human heart failure by impairing cardiac myofilament integration.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Molecular Medicine
Background:
- Ankyrin polypeptides are intracellular proteins crucial for cardiac membrane protein targeting.
- Physiological remodeling of the heart is a complex adaptive response to stress and aging.
Purpose of the Study:
- To investigate the role of ankyrin-G in cardiac remodeling under stress and aging.
- To elucidate the mechanism by which ankyrin-G influences cardiac function.
- To determine the association between ankyrin-G disruption and human heart failure.
Main Methods:
- In vivo studies to assess ankyrin-G function during myocardial stress and aging.
- Mechanistic investigations into ankyrin-G's role in cardiac myofilament integration.
- Analysis of ankyrin-G in human heart failure samples.
Main Results:
- Ankyrin-G plays an unexpected, critical role in compensatory cardiac remodeling.
- Ankyrin-G acts as a nodal protein essential for integrating cardiac myofilaments with the intercalated disc.
- Disruption of ankyrin-G is implicated in the development and progression of human heart failure.
Conclusions:
- Ankyrin-G is necessary for normal cardiac adaptation to stress and aging.
- Ankyrin-G's function in myofilament integration is key to maintaining heart health.
- Ankyrin-G disruption represents a novel mechanism contributing to heart failure pathogenesis.
Keywords:
AnkG, ankyrin-GDSP, desmoplakinECG, electrocardiogramHF, heart failureLV, left ventricularNav1.5PBS, phosphate-buffered salinePKP2, plakophilin-2TAC, transverse aortic constrictionTUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labelingWT, wild-typeankyrinarrhythmiacKO, cardiomyocyte-specific knockoutcytoskeletonheart failureion channel
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