Abstract
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by thrombosis in arteries, veins or small blood vessels, and/or obstetric APS (OAPS), as well as persistent positive antiphospholipid antibodies. In recent years, some authors have proposed that the pathogenesis of APS is closely related to activation of vascular endothelial cells, immune cells, and complement activation. However, further exploration is still needed. Previous studies have shown that the mammalian target of rapamycin (mTOR) is associated with pro-inflammatory and pro-coagulant processes. This indicates that the activation of the mTOR signaling pathway may function as an intermediate mediator, causing immune disorders, thereby leading to thrombosis and OAPS. Therefore, we should correctly understand the potential pathogenic role of the mTOR signaling pathway in APS, which will be more conducive to clinicians' understanding of the pathogenesis of this disease and the search for new therapeutic targets. We hope this can open up a new window for the management of APS.