Remodeling muscles with calcineurin.
Journal Article (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.
- Olson, EN; Williams, RS
- June 2000
Volume / Issue
- 22 / 6
Start / End Page
- 510 - 519
International Standard Serial Number (ISSN)
Digital Object Identifier (DOI)
- United States