Impaired Autophagy Induced by oxLDL/β2GPI/anti-β2GPI Complex through PI3K/AKT/mTOR and eNOS Signaling Pathways Contributes to Endothelial Cell Dysfunction

Figure 9

Proposed model for autophagy inhibition-promoted endothelial cell dysfunction induced by oxLDL/β2GPI/anti-β2GPI complex. OxLDL/β2GPI/anti-β2GPI complex, the circulating immune complex combined by oxLDL/β2GPI complex and anti-β2GPI, could suppress the autophagy process through activating both PI3K/AKT/mTOR and eNOS in endothelial cells. This inhibition would lead to elevated inflammation, oxidative stress, and apoptosis, which finally induced endothelial cell dysfunction. Abbreviations: oxLDL: oxidized low-density lipoprotein; β2GPI: β2-glycoprotein I; anti-β2GPI: anti-β2-glycoprotein I antibody; PI3K: phosphatidylinositol-3 kinase; AKT: serine/threonine kinase; mTOR: the kinase mammalian target of rapamycin; eNOS: endothelial nitric oxide synthase.