Placenta autophagy is closely associated with preeclampsia

Area of Science:

• Reproductive biology
• Molecular genetics
• Immunology

Background:

• Preeclampsia (PE) pathogenesis is complex, with placental autophagy regulating internal homeostasis.
• Limited research exists on placental autophagy's specific role in PE development.

Purpose of the Study:

• To identify key autophagy-related genes and biomarkers for preeclampsia diagnosis.
• To investigate the underlying molecular mechanisms and immune infiltration patterns in PE.

Main Methods:

• Downloaded and analyzed GEO datasets (GSE75010, GSE10588).
• Utilized Limma, WGCNA, Random Forest, and LASSO algorithms to screen differentially expressed and hub genes.
• Constructed a nomogram model for PE diagnosis and analyzed immune cell infiltration.

Main Results:

• Identified 5 autophagy-related hub genes and 3 diagnostic biomarkers: HK2, PLOD2, and TREM1.
• HK2, PLOD2, and TREM1 are implicated in hypoxia-induced autophagy and HIF-1 signaling in PE.
• The nomogram model demonstrated excellent predictive power (AUCs 0.869-0.876).
• PE placentas showed altered immune infiltration (increased CD8+ T cells, decreased M2 macrophages), correlating with biomarker expression.

Conclusions:

• HK2, PLOD2, and TREM1 show potential as diagnostic biomarkers for preeclampsia.
• These biomarkers may play a synergistic role in PE pathogenesis via hypoxia-related pathways.
• Further investigation is needed to elucidate the precise mechanisms of HK2, PLOD2, and TREM1 in preeclampsia.