PREEKLAMPSİ PATOFİZYOLOJİSİNDE ROL OYNAYAN MOLEKÜLER YOLAKLAR

Year 2023, , 380 - 387, 13.07.2023

Damla Gül Fındık , Gülnur Take

https://doi.org/10.18229/kocatepetip.988858

Abstract

Preeklampsi (PE) gebeliklerin yaklaşık % 4-5’inde görülen, hipertansiyon ve üriner proteinüri ile seyreden obstetrik bir hastalıktır. Maternal ve fetal komplikasyonlara neden olabilmektedir. PE alanında çok sayıda yapılan araştırmalara rağmen altta yatan patogenez hala belirsizdir. Ancak ilgili bu araştırmalar ile birlikte PE’yi tetikleyen çok sayıda moleküler mekanizma olduğu sonucuna varılmıştır. Bu moleküler mekanizmalardan yola çıkarak PE iki evrede incelenebilir. İlk evre anormal plasentasyon nedeniyle oluşan plasental iskemidir. İkinci evrede ise iskemik plasentadan dolaşıma salınan nekrotik ve apoptotik faktörler, sistemik inflamasyon ve endotelyal disfonksiyona neden olur. Plasental hücrelerden salınan bu faktörlerden biri de antianjiyogenik faktörlerdir. Ayrıca PE’de antioksidan ve prooksidan mekanizmalarda rekürren iskemi reperfüzyon hasarından dolayı olduğu düşünülen dengesizlik mevcuttur. PE’deki sistemik inflamatuar yanıt maternal immün hücrelerin trofoblastlarla teması sonucu ortaya çıkan immün yanıtla ilişkilendirilmektedir. Bu derlemenin amacı PE'ye giden yolda rol oynayan mevcut moleküler mekanizmaları göstermektir. İlgili moleküler mekanizmaların daha iyi anlaşılması doğrutusunda gelişen PE patogenezine dair yeni görüşler, ilerideki çalışmalara ışık tutacaktır.

Keywords

Preeklampsi, Anjiyogenik proteinler, İnflamasyon, Plasentasyon

MOLECULAR PATHWAYS THAT PLAY A ROLE IN THE PREECLAMPSIA PATHOPHYSIOLOGY

Abstract

Preeclampsia (PE) is an obstetric disease seen in approximately 4-5% of pregnancies progressing with hypertension and urinary proteinuria. It may cause maternal and fetal complications. Despite numerous researches in the field of PE, the underlying pathogenesis remains unclear. However, with these related studies, it has been concluded that there are many molecular mechanisms that trigger PE. Based on these molecular mechanisms, PE can be examined in two stages. The first stage is placental ischemia caused by abnormal placentation. In the second stage, necrotic and apoptotic factors released from the ischemic placenta into the circulation cause systemic inflammation and endothelial dysfunction. One of these factors released from placental cells is the antiangiogenic factor. Also, there is an imbalance in the antioxidant and prooxidant mechanisms that are thought to be due to recurrent ischemia reperfusion injury in PE. The systemic inflammatory response in PE is associated with the immunological response resulting from the contact of the maternal immune cells with trophoblasts. The aim of this review is to present the current molecular mechanisms implicating the pathway leading to PE. The development of new insights into the pathogenesis of PE in conclusion of a better understanding of the relevant molecular mechanisms will guide further studies.

Keywords

Preeclampsia, Angiogenic Proteins, Inflammation, Placentation

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