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In Vivo Modeling of the Morbid Human Genome using Danio rerio

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Published on: August 24, 2013

Thin filament mutations: developing an integrative approach to a complex disorder.

Jil C Tardiff¹

¹Department of Physiology and Biophysics, Department of Internal Medicine, Division of Adult Cardiology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. j.tardiff@einstein.yu.edu

Circulation Research

|March 19, 2011

Summary

Familial hypertrophic cardiomyopathy is linked to mutations in cardiac sarcomere components. This review focuses on thin filament cardiomyopathies, exploring genotype-phenotype links for better patient management.

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Area of Science:

Cardiovascular Research
Genetics
Molecular Biology

Background:

Familial hypertrophic cardiomyopathy was redefined as a cardiac sarcomere disease following discoveries of mutations in cardiac troponin T and α-tropomyosin.
Thin filament mutations cause heterogeneous ventricular remodeling and varied clinical presentations.

Purpose of the Study:

To examine biophysical and clinical evidence supporting a proximal definition of thin filament cardiomyopathies.
To present integrated approaches for linking genotype to phenotype in this complex disorder.

Main Methods:

Review of existing biophysical and clinical evidence.
Discussion of high-resolution, integrated research approaches.

Main Results:

Nearly 100 mutations identified across all cardiac thin filament components.
Evidence suggests thin filament cardiomyopathies are progressive.

Conclusions:

A renewed focus on proximal molecular and clinical events is crucial for managing thin filament cardiomyopathies.
Developing robust genotype-phenotype correlations is essential for patient care.