Molecular Mechanisms of Fabry Disease

This template shows how Gb3 accumulation in mitochondria, endosomes, and caveolae of the vascular endothelium leads to excessive ROS production, microparticle release that activates neutrophils and triggers myeloperoxidase release, and increased adhesin levels (P-selectin, ICAM-1, VCAM-1) that activate leukocytes. It also traces increased tPA/uPA levels driving plasmin generation and an imbalance between coagulation and fibrinolysis, culminating in a prothrombotic state that raises stroke risk.

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