Molecular Pathways of Altered Brain Development in Fetuses Exposed to Hypoxia.

Autor: Orzeł A; Centre of Postgraduate Medical Education, I-st Department of Obstetrics and Gynecology, 01-813 Warsaw, Poland., Unrug-Bielawska K; Department of Genetics, Maria Sklodowska-Curie National Research Institute of Oncology, 00-001 Warsaw, Poland., Filipecka-Tyczka D; Centre of Postgraduate Medical Education, I-st Department of Obstetrics and Gynecology, 01-813 Warsaw, Poland., Berbeka K; Centre of Postgraduate Medical Education, I-st Department of Obstetrics and Gynecology, 01-813 Warsaw, Poland., Zeber-Lubecka N; Department of Genetics, Maria Sklodowska-Curie National Research Institute of Oncology, 00-001 Warsaw, Poland.; Centre of Postgraduate Medical Education, Department of Gastroenterology, Hepatology and Clinical Oncology, 01-813 Warsaw, Poland., Zielińska M; Centre of Postgraduate Medical Education, I-st Department of Obstetrics and Gynecology, 01-813 Warsaw, Poland., Kajdy A; Centre of Postgraduate Medical Education, I-st Department of Obstetrics and Gynecology, 01-813 Warsaw, Poland.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2023 Jun 20; Vol. 24 (12). Date of Electronic Publication: 2023 Jun 20.
DOI: 10.3390/ijms241210401
Abstrakt: Perinatal hypoxia is a major cause of neurodevelopmental impairment and subsequent motor and cognitive dysfunctions; it is associated with fetal growth restriction and uteroplacental dysfunction during pregnancy. This review aims to present the current knowledge on brain development resulting from perinatal asphyxia, including the causes, symptoms, and means of predicting the degree of brain damage. Furthermore, this review discusses the specificity of brain development in the growth-restricted fetus and how it is replicated and studied in animal models. Finally, this review aims at identifying the least understood and missing molecular pathways of abnormal brain development, especially with respect to potential treatment intervention.
Databáze: MEDLINE
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