Remodeling muscles with calcineurin

Eric N. Olson, R. Sanders Williams

Research output: Contribution to journalReview article

215 Scopus citations

Abstract

Ca2+ 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 Ca2+ in the cytoplasm activate the hypertrophic response and result in longterm changes in muscle gene expression are unclear. The Ca2+, calmodulin-dependent protein phosphatase calcineurin has been proposed to control cardiac and skeletal muscle hypertrophy by acting as a Ca2+ sensor that couples prolonged changes in Ca2+ 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 Ca2+ 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 Ca2+-regulated gene expression in muscle cells and discuss potential implications of these findings for pharmacologic modification of cardiac and skeletal muscle function. (C) 2000 John Wiley and Sons, Inc.

Original languageEnglish (US)
Pages (from-to)510-519
Number of pages10
JournalBioEssays
Volume22
Issue number6
DOIs
StatePublished - Jan 1 2000

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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