Journal of Molecular Medicine

, Volume 76, Issue 11, pp 725–746

Cellular mechanisms of cardiac hypertrophy

  • P. H. Sugden
  • Angela Clerk
Review

DOI: 10.1007/s001090050275

Cite this article as:
Sugden, P. & Clerk, A. J Mol Med (1998) 76: 725. doi:10.1007/s001090050275

Abstract

Hypertrophy of myocytes in the heart ventricles is an important adaptation that in vivo occurs in response to a requirement for increased contractile power. It involves changes at the level of gene transcription, stimulation of the rate of protein synthesis (translation), and increased assembly of myofibrils. There is mounting evidence of the involvement of reversible protein phosphorylation and dephosphorylation in most of these processes. Protein kinase C, mitogen-activated protein kinases, and transcription factors have been implicated in the modulation of the transcriptional changes. Activation of translation may also be mediated through protein phosphorylation/dephosphorylation, although this has not been clearly established in the heart. Here we provide a critical overview of the signalling pathways involved in the hypertrophic response and provide a scheme to account for many of its features.

Key words Ventricular myocytesEndothelinα1-Adrenergic stimulationProtein kinasesTranscriptionTranslation

Copyright information

© Springer-Verlag Berlin Heidelberg 1998

Authors and Affiliations

  • P. H. Sugden
    • 1
  • Angela Clerk
    • 2
  1. 1.National Heart and Lung Institute Division (Cardiac Medicine), Imperial College School of Medicine, Royal Brompton Campus, Dovehouse Street, London SW3 6LY, UKGB
  2. 2.Division of Biomedical Sciences (Molecular Pathology), Imperial College School of Medicine, South Kensington Campus, Exhibition Road, London SW6 2LZ, UKGB