Remodeling muscles with calcineurin.

Journal Article (Review)

Ca(2+) signaling plays a central role in hypertrophic growth of cardiac and skeletal muscle in response to mechanical load and a variety of signals. However, the mechanisms whereby alterations in Ca(2+) in the cytoplasm activate the hypertrophic response and result in longterm changes in muscle gene expression are unclear. The Ca(2+), calmodulin-dependent protein phosphatase calcineurin has been proposed to control cardiac and skeletal muscle hypertrophy by acting as a Ca(2+) sensor that couples prolonged changes in Ca(2+) levels to reprogramming of muscle gene expression. Calcineurin also controls the contractile and metabolic properties of skeletal muscle by activating the slow muscle fiber-specific gene program, which is dependent on Ca(2+) signaling. Transcription factors of the NFAT and MEF2 families serve as endpoints for the signaling pathways whereby calcineurin controls muscle hypertrophy and fiber-type. We consider these findings in the context of a model for Ca(2+)-regulated gene expression in muscle cells and discuss potential implications of these findings for pharmacologic modification of cardiac and skeletal muscle function. BioEssays 22:510-519, 2000.

Full Text

Duke Authors

Cited Authors

  • Olson, EN; Williams, RS

Published Date

  • June 2000

Published In

Volume / Issue

  • 22 / 6

Start / End Page

  • 510 - 519

PubMed ID

  • 10842305

International Standard Serial Number (ISSN)

  • 0265-9247

Digital Object Identifier (DOI)

  • 10.1002/(SICI)1521-1878(200006)22:6<510::AID-BIES4>3.0.CO;2-1

Language

  • eng

Conference Location

  • United States