Heart failure: Targeting transcriptional and post-transcriptional control mechanisms of hypertrophy for treatment

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Abstract

Heart failure (HF) is a syndrome caused by diminished heart function that arises from pathologies like hypertension, infarction, and diabetes. Neurohormonal, cardiorenal and cardiocirculatory models have been developed to explain HF but they have not provided sufficient understanding for the elaboration of therapies to conquer the syndrome. In fact, even though progress has been made in improving survival, HF remains a frequent cause of hospitalization and death. Since in most forms of HF, development of the disorder is associated with an alteration of cardiomyocyte structure, perceived as an increase in heart mass due to cell hypertrophy, effort is being directed to address hypertrophy as a therapeutic target. Here, we outline recent understanding of two gene-silencing regulatory mechanisms underlying cardiomyocyte hypertrophy, i.e., transcriptional control by HDACs, and post-transcriptional control by microRNAs.

Original languageEnglish
Pages (from-to)1643-1648
Number of pages6
JournalInternational Journal of Biochemistry and Cell Biology
Volume40
Issue number9
DOIs
Publication statusPublished - 2008

Keywords

  • Heart failure
  • Histone deacetylase
  • Hypertrophy
  • MicroRNA

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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