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.
Highlights
Epigenetics is defined as heritable changes in gene expression that do not result from a change in the DNA sequence [1]
There is an urgent need for new therapies for neonatal HI, as currently, therapeutic hypothermia for term infants is not fully protective against hypoxic-ischemic encephalopathy (HIE), and the disability burden after neonatal HI remains high
The cellular hypoxia response, mediated by hypoxia inducible factor (HIF)-1α and other hypoxia-inducible factors, is controlled by an intricate multi-leveled epigenetic network centered on HIF-1a
Summary
Epigenetics is defined as heritable changes in gene expression that do not result from a change in the DNA sequence [1]. HIF-1 expression levels, protein stabilization, and its association with HRE are under tight epigenetic regulation, including promoter methylation and microRNA (miRNAs) control [30,31,32].
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