Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C Signaling

Abstract

Background: Chronic PKC activation is the leading pathogenic component of diabetes in the heart. Results: PKCα/β promotes fetal splicing patterns in adult diabetic hearts via phosphorylation of the RNA-binding proteins CELF1 and Rbfox2. Conclusion: PKCα/β contributes to diabetes pathogenesis by manipulating developmentally regulated alternative splicing. Significance: Identifying downstream effectors of PKC can provide novel therapeutics for cardiac pathogenesis of diabetes. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.