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

研究成果: ジャーナルへの寄稿評論記事

44 引用 (Scopus)

抄録

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.

元の言語英語
ページ(範囲)785-791
ページ数7
ジャーナルJournal of Molecular Medicine
87
発行部数8
DOI
出版物ステータス出版済み - 8 1 2009

Fingerprint

Histone Deacetylases
Cardiomegaly
Oxidation-Reduction
Thioredoxins
Cell Nucleus Active Transport
Hypertrophy
Cysteine
Protamine Kinase
NFATC Transcription Factors
Post Translational Protein Processing
Oxidants
Transcription Factors
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)

これを引用

The role of redox modulation of class II histone deacetylases in mediating pathological cardiac hypertrophy. / Oka, Shin Ichi; Ago, Tetsuro; Kitazono, Takanari; Zablocki, Daniela; Sadoshima, Junichi.

:: Journal of Molecular Medicine, 巻 87, 番号 8, 01.08.2009, p. 785-791.

研究成果: ジャーナルへの寄稿評論記事

@article{05bcc51693ee4198a9b2e5db9a9e5184,
title = "The role of redox modulation of class II histone deacetylases in mediating pathological cardiac hypertrophy",
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.",
author = "Oka, {Shin Ichi} and Tetsuro Ago and Takanari Kitazono and Daniela Zablocki and Junichi Sadoshima",
year = "2009",
month = "8",
day = "1",
doi = "10.1007/s00109-009-0471-2",
language = "English",
volume = "87",
pages = "785--791",
journal = "Clinical Investigator",
issn = "0946-2716",
publisher = "Springer Verlag",
number = "8",

}

TY - JOUR

T1 - The role of redox modulation of class II histone deacetylases in mediating pathological cardiac hypertrophy

AU - Oka, Shin Ichi

AU - Ago, Tetsuro

AU - Kitazono, Takanari

AU - Zablocki, Daniela

AU - Sadoshima, Junichi

PY - 2009/8/1

Y1 - 2009/8/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=70349251897&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70349251897&partnerID=8YFLogxK

U2 - 10.1007/s00109-009-0471-2

DO - 10.1007/s00109-009-0471-2

M3 - Review article

C2 - 19424677

AN - SCOPUS:70349251897

VL - 87

SP - 785

EP - 791

JO - Clinical Investigator

JF - Clinical Investigator

SN - 0946-2716

IS - 8

ER -