Antiphospholipid syndrome (APS) is a systemic autoimmune disorder leading to recurrent thromboembolic events and pregnancy morbidity. It is driven by antiphospholipid antibodies (aPL), such as anti-cardiolipin and anti-β2-glycoprotein I (anti-β2GPI), which are known to induce endothelial dysfunction. Similar processes to those triggered by aPL in APS can also lead to the shedding of endothelial glycocalyx (eGC), a structure essential to maintaining vascular homeostasis. Disruption of the eGC in and of itself leads to vascular inflammation and thrombosis. Its contribution to APS pathogenesis, however, remains poorly defined, with limited evidence suggesting eGC impairment in APS patients.
The aim of this research project is to determine whether aPL directly induce eGC shedding. Elucidating this pathway may identify novel biomarkers of disease activity and therapeutic strategies supporting the preservation of vascular integrity in patients with APS.
To reach these goals, the following research questions have been defined: To assess eGC degradation in APS patients and correlate eGC loss with endothelial dysfunction and disease severity. To investigate whether anti-β2GPI and anti-cardiolipin antibodies directly induce eGC shedding and dysfunction. To determine how eGC shedding contributes to thrombosis and vascular inflammation in APS. To explore therapeutic strategies to protect or restore the eGC.