Cytoskeletal defects in cardiomyopathy

Elizabeth McNally*, Michael Allikian, Matthew T. Wheeler, John M. Mislow, Ahlke Heydemann

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

22 Scopus citations

Abstract

Genetic studies of cardiomyopathy and muscular dystrophy have emphasized the importance of the striated myocyte cytoskeleton. Cytoskeletal defects produce myopathies through a combination of structural and signaling mechanisms. Broadly, the cytoskeletal proteins defective in these myopathic syndromes can be classified into categories based on their intracellular locations. The first category includes proteins of the plasma membrane that interact with both subsarcolemmal and extracellular matrix proteins. The second category, generally associated with hypertrophic cardiomyopathies, includes proteins of the sarcomere. The last, newly emerging, category includes proteins of the inner nuclear membrane. In this review, we will examine the genetic defects that lead to cardiomyopathy and the potential means by which these varied proteins normally maintain the structural integrity of myocytes.

Original languageEnglish (US)
Pages (from-to)231-241
Number of pages11
JournalJournal of Molecular and Cellular Cardiology
Volume35
Issue number3
DOIs
StatePublished - Mar 1 2003

Keywords

  • Cardiomyopathy
  • Cytoskeleton
  • Dystroglycan
  • Dystrophin
  • Emerin
  • Extracellular matrix
  • Lamin
  • Nuclear membrane
  • Sarcoglycan
  • Sarcolemma
  • Sarcomere
  • Titin
  • Z-line

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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