Leveraging PANoptosis-associated genes for unraveling implication of decidualization deficiency in pre-eclampsia via transcriptome data and experiment validation - PubMed

7 hours ago

The study explores the association between PANoptosis-related genes and decidualization deficiency in pre-eclampsia (PE).
430 differentially expressed genes (DEGs) were identified, mainly involved in inflammation, apoptosis, and decidual tissue dysfunction in PE.
10 PANoptosis-related DEGs were screened, with immune landscape analysis revealing aberrant immunocyte abundance and immune checkpoint levels in PE decidual tissue.
Nine PANoptosis-related signature genes (MAPK3, RIPK1, RIPK3, PYCARD, BAX, TUG1, CDK1, MAPK1, TAB2) were identified using machine learning algorithms.
Artificial neural network (ANN) and nomogram models showed high discriminative ability (AUC = 0.999).
Validation in primary human decidual stromal cells (HDSCs) confirmed dysregulated expression of signature genes and reduced decidualization markers (PRL, IGFBP1).
Two PE subtypes were identified, with subtype B showing immune hyperactivity compared to subtype A.
Melatonin was identified as a candidate therapeutic compound, showing protective effects in vivo and in vitro.
MAPK3 knockdown attenuated PANoptosis-associated inflammatory cytokine production and partially restored decidualization markers.
The study suggests PANoptosis-related molecular dysregulation may contribute to decidualization deficiency in PE, with potential biomarkers and therapeutic targets identified.

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