The biology of preeclampsia

Abstract

Preeclampsia is a systemic disease that results from placental defects and occurs in about 5–8% of pregnancies worldwide. Preeclampsia is a disease of many theories, wherein investigators put forward their favorite mechanistic ideas, each with a causal appeal for the pathogenesis of preeclampsia. In reality, the patho-mechanism of preeclampsia remains largely unknown. Preeclampsia, as diagnosed in patients today, is likely a heterogeneous collection of disease entities that share some common features but also exhibit important differences. Therefore, one single mechanism may never be found to explain all the variants of preeclampsia. Current research must focus on evaluating such diverse mechanisms, as well as the possible common effectors pathways. Here we provide a discussion of several possible mechanisms and putative theories proposed for preeclampsia, with particular emphasis on the recent discovery of a new genetic mouse model offering new opportunities to explore experimental therapies.

MicroRNA‐181a Regulates Local Immune Balance by Inhibiting Proliferation and Immunosuppressive Properties of Mesenchymal Stem Cells

“…Its pathogenesis is not completely understood. Previous studies indicate that PE may be a pregnancy-induced autoimmune disease, and that the unbalanced immune system in the maternal-fetal interface may be one cause of PE [8][9][10]. Maternal-fetal interface is an important source of Author contributions: L.L.…”

Preeclampsia Y Sus Principales Factores De Riesgo

“…La naturaleza de distribución familiar de la preeclampsia ha sido suficientemente demostrada; se considera que el riesgo de desarrollar preeclampsia durante el embarazo, aumenta dos a cinco veces en parientes de primer grado de mujeres afectadas 17 .…”

Las Dos Caras De La Inmunidad: Respuesta Th

“…El remodelado vascular a través de la invasión de trofoblasto extravelloso, incluye el reemplazo de células musculares lisas de las arterias espirales. La consecuencia de una circulación placentaria adecuada permite un gran flujo sanguíneo, una baja resistencia y una menor velocidad del flujo sanguíneo a nivel del espacio intervelloso (que evita el flujo turbulento, disminuye el "shear stress" y maximiza el intercambio por difusión) 11,12 .…”