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REV-ERBα Ameliorates Heart Failure Through Transcription Repression

ABSTRACT: Heart failure remains a major unmet clinical need and current therapies targeting neurohomonal and hemodynamic regulation have limited efficacy. We report that pharmacological activation of the transcriptional repressor REV-ERBa prevents expression of a pathological gene program and cardiomyocyte hypertrophy. In vivo, REV-ERBa agonism prevents development and halts progression of heart failure in mouse models. Thus, modulation of gene networks by targeting REV-ERBa represents a novel approach to heart failure therapy.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE98575 | GEO | 2017/09/11

SECONDARY ACCESSION(S): PRJNA385542

REPOSITORIES: GEO

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REV-ERBa and REV-ERBb function as key factors regulating Mammalian Circadian Output

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