Antiphospholipid Antibodies Increase Endometrial Stromal Cell Decidualization, Senescence and Inflammation via TLR4, ROS and p38 MAP Kinase Signaling

Antiphospholipid autoantibodies increased human endometrial stromal cell decidualization, senescence and inflammation. The decidualization and inflammatory responses were partially mediated by toll-like receptor 4 (TLR4) and p38 MAP kinase, while the decidualization and senescence responses were reactive oxygen species (ROS)-dependent.