Autor: |
Vrzić Petronijević S; University of Belgrade, Faculty of Medicine, University Clinical Center of Serbia Clinic for Obstetrics and Gynecology, Koste Todorovića 26, 11000 Belgrade, Serbia., Vilotić A; University of Belgrade, Institute for the Application of Nuclear Energy, Department for Biology of Reproduction, Banatska 31b, 11080 Belgrade, Serbia., Bojić-Trbojević Ž; University of Belgrade, Institute for the Application of Nuclear Energy, Department for Biology of Reproduction, Banatska 31b, 11080 Belgrade, Serbia., Kostić S; University of Belgrade, Faculty of Medicine, University Clinical Center of Serbia Clinic for Obstetrics and Gynecology, Koste Todorovića 26, 11000 Belgrade, Serbia., Petronijević M; University of Belgrade, Faculty of Medicine, University Clinical Center of Serbia Clinic for Obstetrics and Gynecology, Koste Todorovića 26, 11000 Belgrade, Serbia., Vićovac L; University of Belgrade, Institute for the Application of Nuclear Energy, Department for Biology of Reproduction, Banatska 31b, 11080 Belgrade, Serbia., Jovanović Krivokuća M; University of Belgrade, Institute for the Application of Nuclear Energy, Department for Biology of Reproduction, Banatska 31b, 11080 Belgrade, Serbia. |
Abstrakt: |
Antiphospholipid syndrome (APS) is a complex thrombo-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL). Women with APS are at high risk of recurrent early pregnancy loss as well as late obstetrical complications-premature birth due to placental insufficiency or severe preeclampsia. Accumulating evidence implies that vascular thrombosis is not the only pathogenic mechanism in obstetric APS, and that the direct negative effect of aPL on the placental cells, trophoblast, plays a major role. In this review, we summarize the current findings regarding the potential mechanisms involved in aPL-induced trophoblast dysfunction. Introduction on the APS and aPL is followed by an overview of the effects of aPL on trophoblast-survival, cell function and aPL internalization. Finally, the implication of several non-coding RNAs in pathogenesis of obstetric APS is discussed, with special emphasis of their possible role in trophoblast dysfunction and the associated mechanisms. |