Abstract:

Preeclampsia (PE) is a common complication during pregnancy. The pathogenesis of PE is closely related to immune imbalance, inflammatory responses, and placental dysfunction. The triggering receptors expressed on myeloid cells-1 (TREM-1) is an important pro-inflammatory receptor, widely expressed in neutrophils and mononuclear macrophages. TREM-1 plays a role in amplifying inflammatory responses in various inflammatory diseases. Studies have found that TREM-1 expression is significantly elevated in the peripheral blood and placental tissues of PE patients. It can activate nuclear factor-κB (NF-κB) and promote the release of cytokines through the multiple signaling pathways such as DNAX-associated protein 12 (DAP12), Toll-like receptor 4 (TLR4), and nucleotide-binding oligomerization domain receptors (NLRs), thereby exacerbating inflammatory damage and endothelial dysfunction. TREM-1 may also serve as a potential biomarker for the early assessment of PE risk and severity. This review focuses on the structure of TREM-1, its signaling pathways and possible mechanisms in the development of PE, aiming to provide a theoretical basis for the early diagnosis and targeted intervention of PE.

Key words: Pre-eclampsia, Inflammation, Oxidative stress, Signal transduction, Triggering receptor expressed on myeloid cells-1