Clinical Implications of Epigenetic Dysregulation in Perinatal Hypoxic-Ischemic Brain Damage

Martin Bustelo, Melinda Barkhuizen, Daniel L. A. van den Hove, Harry Wilhelm M. Steinbusch, Martn A. Bruno, C. Fabian Loidl, Antonio W. Danilo Gavilanes*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

15 Citations (Web of Science)

Abstract

Placental and fetal hypoxia caused by perinatal hypoxic-ischemic events are major causes of stillbirth, neonatal morbidity, and long-term neurological sequelae among surviving neonates. Brain hypoxia and associated pathological processes such as excitotoxicity, apoptosis, necrosis, and inflammation, are associated with lasting disruptions in epigenetic control of gene expression contributing to neurological dysfunction. Recent studies have pointed to DNA (de)methylation, histone modifications, and non-coding RNAs as crucial components of hypoxic-ischemic encephalopathy (HIE). The understanding of epigenetic dysregulation in HIE is essential in the development of new clinical interventions for perinatal HIE. Here, we summarize our current understanding of epigenetic mechanisms underlying the molecular pathology of HI brain damage and its clinical implications in terms of new diagnostic, prognostic, and therapeutic tools.

Original languageEnglish
Article number483
Number of pages15
JournalFrontiers in Neurology
Volume11
DOIs
Publication statusPublished - 9 Jun 2020

Keywords

  • hypoxic-ischemic encephalopathy
  • biomarker
  • hypoxia
  • ischemia
  • microRNAs
  • histone modifications
  • DNA methylation
  • HUMAN ENDOTHELIAL-CELLS
  • LONG NONCODING RNAS
  • NEONATAL BRAIN
  • INDUCIBLE FACTOR
  • DNA METHYLATION
  • GENE-EXPRESSION
  • PROVIDES NEUROPROTECTION
  • HISTONE DEMETHYLASES
  • HUMAN PLACENTAS
  • DOWN-REGULATION

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