The role of redox modulation of class II histone deacetylases in mediating pathological cardiac hypertrophy

Shin Ichi Oka, Tetsuro Ago, Takanari Kitazono, Daniela Zablocki, Junichi Sadoshima

Research output: Contribution to journalReview articlepeer-review

50 Citations (Scopus)

Abstract

Many biological functions in cells are regulated by the effects of the redox state on cellular signaling pathways. In the heart, pathological hypertrophy caused by a wide variety of stimuli is commonly mediated by nucleo-cytoplasmic translocation of class II histone deacetylases (HDACs) and subsequent de-suppression of transcription factors, including nuclear factor of activated T-cells and MEF2. One of the primary triggers of class II HDAC nuclear export is phosphorylation by HDAC kinases activated by hypertrophic stimuli. However, oxidative modification of conserved cysteine residues can also potentially induce nuclear export of class II HDACs. Thioredoxin 1 (Trx1), a 12 kDa anti-oxidant, inhibits pathological hypertrophy through reduction of cysteine residues in class II HDACs. In this review, we discuss the role of posttranslational modification of class II HDACs in mediating cardiac hypertrophy and the molecular mechanism by which Trx1 inhibits pathological cardiac hypertrophy.

Original languageEnglish
Pages (from-to)785-791
Number of pages7
JournalJournal of Molecular Medicine
Volume87
Issue number8
DOIs
Publication statusPublished - Aug 2009

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)

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