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Cardiomyopathies and Related Changes in Contractility of Human Heart Muscle

Petr G Vikhorev1, Natalia N Vikhoreva2

  • 1National Heart and Lung Institute, Imperial College London, London W12 0NN, UK. p.vikhorev@imperial.ac.uk.

International Journal of Molecular Sciences
|August 2, 2018
PubMed

Insights

Genetic mutations in sarcomeric and non-sarcomeric proteins cause cardiomyopathies by affecting heart muscle contractility. Further research is needed to fully understand how these genetic defects lead to disease progression.

Area of Science:

  • Cardiology
  • Genetics
  • Molecular Biology

Background:

  • Cardiomyopathies, including hypertrophic and dilated forms, are often genetic.
  • Sarcomeric proteins are crucial for cardiomyocyte contractility and structure.
  • Non-sarcomeric protein mutations can alter cell signaling and cardiac function.

Purpose of the Study:

  • To review the role of cardiac myofilament contractility in cardiomyopathy.
  • To explore the link between genetic mutations and contractile dysfunction in heart failure.

Main Methods:

  • Literature review of studies on genetic cardiomyopathies.
  • Analysis of research on sarcomeric and non-sarcomeric protein function.
  • Examination of data on cardiac myofilament mechanics in patients.

Main Results:

  • Approximately 50% of cardiomyopathy cases are linked to sarcomeric protein mutations.
  • Contractile dysfunction is a central feature in the initiation and progression of cardiomyopathies.
  • Abnormalities in myofibril contractile mechanics are evident in affected individuals.

Conclusions:

  • Genetic mutations significantly impact cardiac contractility, contributing to cardiomyopathy development.
  • Understanding the precise mechanisms by which mutations cause disease remains an active area of research.

Keywords:
Ca2+-sensitivitycardiomyopathy mutationsdilated cardiomyopathyhuman heart muscle contractilityhypertrophic cardiomyopathylength dependent activationtroponin phosphorylation

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