Молекулярные механизмы преэклампсии: ОБЗОРЫ

Иван Александрович  Ершов; Андрей Глебович  Васильев; Виталий Анатольевич  Резник; Анна Николаевна  Тайц; Елена Александровна  Шкунова; Юлия Валерьевна  Кошкина; Наталья Ивановна  Агалакова

doi:10.56871/PED.2025.25.75.007

Molecular mechanisms of preeclampsia

REVIEWS

Ivan A. Ershov Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Andrey G. Vasiliev Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Vitaly A. Reznik Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Anna N. Taits Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Elena A. Shkunova Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Yuliya V. Koshkiva Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia
Natalia I. Agalakova Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, Saint Petrsburg, Russia

Keywords:

преэклампсия антиангиогенные факторы фетоплацентарные молекулы иммунологические реакции эпигенетические механизмы профибротические факторы preeclampsia antiangiogenic factors fetoplacental molecules immunological reactions epigenetic mechanisms profibrotic factors

Abstract

Preeclampsia (PE) is one of the major obstetric syndromes, manifested by a persistent increase in blood pressure and associated complications, and in severe cases — by systemic damage to the organs of mother and fetus. Due to complexity of the etiology of this disease, key and reliable molecular markers that could be used as predictors for early diagnostics of PE or as therapeutic targets for its treatment have not been found yet. This review analyzes the data accumulated to date on the most important molecular processes underlying the development of PE — an imbalance between the synthesis of proangiogenic and antiangiogenic factors (soluble fms-like tyrosine kinase sFlt-1, endoglin Eng, placental growth factor PlGF and vascular endothelial growth factor VEGF), fetoplacental molecules (PAPP-A and PP-13), disturbances of immunological reactions (T-helper lymphocytes TH, killer cells uNK, TLRs receptors), genetic and epigenetic mechanisms (abnormal expression of miRNA, circRNA, lncRNA), activation of the effectors of the profibrotic signaling pathway of the cardiotonic steroid marinobufagenin and transcription factor Fli1. Current data highlights the complex profile of the etiology and pathogenesis of PE. Alteration in the balance of pro- and anti-angiogenic factors may be one of the earliest molecular mechanisms underlying abnormal placentation and placental ischemia. Disruption of epigenetic mechanisms regulating placentation and vascular growth, particularly abnormal alterations in the expression of several types of microRNAs, also play an important role in the development of PE. Further development of pathophysiological events associated with adverse pregnancy outcomes in PE includes oxidative stress and immune responses, as well as the development of vascular fibrosis.

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