Pathophysiology of perinatal hypoxic-ischemic encephalopathy - biomarkers, animal models and treatment perspectives
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
28006936
DOI
10.33549/physiolres.933541
PII: 933541
Knihovny.cz E-resources
- MeSH
- Biomarkers metabolism MeSH
- Humans MeSH
- Disease Models, Animal * MeSH
- Hypoxia-Ischemia, Brain metabolism physiopathology therapy MeSH
- Oxidative Stress physiology MeSH
- Pregnancy MeSH
- Treatment Outcome MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Biomarkers MeSH
Hypoxic-ischemic encephalopathy (HIE) is one of the leading pediatric neurological conditions causing long-term disabilities and socio-economical burdens. Nearly 20-50 % of asphyxiated newborns with HIE die within the newborn period and another third will develop severe health consequences and permanent handicaps. HIE is the result of severe systemic oxygen deprivation and reduced cerebral blood flow, commonly occurring in full-term infants. Hypoxic-ischemic changes trigger several molecular and cellular processes leading to cell death and inflammation. Generated reactive oxygen species attack surrounding cellular components resulting in functional deficits and mitochondrial dysfunction. The aim of the present paper is to review present knowledge about the pathophysiology of perinatal hypoxic-ischemic encephalopathy, especially with respect to novel treatment strategies and biomarkers that might enhance early detection of this disorder and thus improve the general outcome of patients.
References provided by Crossref.org
Serum biomarkers of hypoxic-ischemic brain injury
Impact of prenatal hypoxia on the development and behavior of the rat offspring
Perinatal hypoxic-ischemic damage: review of the current treatment possibilities
Impact of perinatal hypoxia on the developing brain