| Autor: |
Kovács P; Clinical Research Unit Hungary Szikszó., Rab A; Landeskrankenhaus Feldkirch Austria., Szentpéteri I; Praxis für Gynäkologie und Geburtshilfe und allgemeine Medizin Wehingen, Baden-Württemberg, Germany., Joó JG; I. Szülészeti és Nőgyógyászati Klinika, Semmelweis Egyetem, Általános Orvostudományi Kar Budapest, Baross u. 27., 1088., Kornya L; Szülészet-Nőgyógyászati Osztály, Egyesített Szent István és Szent László Kórház Budapest. |
| Jazyk: |
maďarština |
| Zdroj: |
Orvosi hetilap [Orv Hetil] 2017 Apr; Vol. 158 (16), pp. 612-617. |
| DOI: |
10.1556/650.2017.30622 |
| Abstrakt: |
Placental vascular endothelial growth factor A (VEGF-A) gene and endoglin gene are both overexpressed in placental samples obtained from pregnancies with intrauterine growth restriction compared to normal pregnancies. In the background of these changes a mechanism can be supposed, in which the increased endoglin activity in intrauterine growth restriction (IUGR) leads to impaired placental circulation through an antioangiogenetic effect. This results in the development of placental vascular dysfunction and chronic fetal hypoxia. It is chronic hypoxia that turns on VEGF-A as a compensatory mechanism to improve fetal vascular blood supply by promoting placental blood vessel formation. Although the maternal serum placental growth factor (PlGF) level is a potential predictor for both IUGR and praeeclampsia, placental PlGF gene activity may be less of an active in the regulation of placental circulation in IUGR pregnancies during the later stages of gestation. Orv. Hetil., 2017, 158(16), 612-617. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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