Pflügers Archiv

, Volume 446, Issue 1, pp 1–8 | Cite as

The role of tropomyosin in the regulation of myocardial contraction and relaxation

  • Beata M. Wolska
  • David F. Wieczorek
Invited Review


Studies over the last 30 years have demonstrated the essential nature of the evolutionarily highly conserved tropomyosin (TM) protein. TM-deficient cells neither function properly nor survive, and mutations within this protein impair severely its function within the sarcomere. The ability to manipulate TM isoform expression genetically within functioning cardiomyocytes and the whole heart has proven essential in deciphering the physiological significance of the different TM isoforms. It is now apparent that α-TM and actin serve as the requisite backbone of the thin filament, with varying levels of β- and γ-TM, together with the troponin complex serving to modulate sarcomere function. Defining the mechanisms whereby specific TM isoform amino acid differences alter thin filament dynamics will enhance greatly the understanding of muscle contraction during both normal and pathological states.

Tropomyosin FHC Thin filament Myocardial contraction Myocardial relaxation 


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Copyright information

© Springer-Verlag 2003

Authors and Affiliations

  • Beata M. Wolska
    • 1
  • David F. Wieczorek
    • 2
  1. 1.Department of Medicine, Section of Cardiology, and Department of Physiology and Biophysics, and Program in Cardiovascular Sciences, College of Medicine, University of Illinois at Chicago, 840 S. Wood St. (M/C 715), Chicago, IL 60612, USA
  2. 2.Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, Cincinnati, OH 45267, USA

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