HDAC4 in ischemic stroke: mechanisms and therapeutic potential

Clin Epigenetics. 2018 Sep 12;10(1):117. doi: 10.1186/s13148-018-0549-1.

Abstract

Stroke is one of the leading causes of death and disability worldwide, and the majority of the cases are ischemic stroke. However, it still lacks effective treatment except for thrombolytic therapy in an extremely narrow time window. Increased evidence suggests that histone deacetylase 4 (HDAC4) was dysregulated in ischemic stroke, which plays a key role in the pathogenesis of ischemic stroke and post-stroke recovery by affecting neuronal death, angiogenesis, and neurogenesis. Therefore, we aim to review the dysregulation of HDAC4 in ischemic stroke and the role of dysregulated HDAC4 in the pathogenesis of ischemic stroke. Furthermore, the therapeutic potential of modulating HDAC4 in ischemic stroke is discussed.

Keywords: Angiogenesis; Cell death; HDAC4; Ischemic stroke; Neurogenesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Brain Ischemia / drug therapy
  • Brain Ischemia / genetics*
  • Down-Regulation
  • Epigenesis, Genetic
  • Histone Deacetylase Inhibitors / therapeutic use
  • Histone Deacetylases / genetics*
  • Humans
  • Neurogenesis
  • Repressor Proteins / genetics*
  • Stroke / drug therapy
  • Stroke / genetics*

Substances

  • Histone Deacetylase Inhibitors
  • Repressor Proteins
  • HDAC4 protein, human
  • Histone Deacetylases