Research Paper Advance Articles

NFAT5 directs hyperosmotic stress-induced fibrin deposition and macrophage infiltration via PAI-1 in endothelium

The schematic diagram shows the process of fibrin deposition, macrophage infiltration and atherosclerosis formation. Stage I: Hypertonicity → NFAT5-dependent PAI-1 gene transcription → PAI-1 secretion. Stage II: PAI-1 secretion → Antifibrinolytic activation/adhesive molecules → Fibrin deposition/monocytes adhesion and infiltration. Stage III: Endothelial dysfunction leads to fibrin deposition, macrophage-driven foam cells and phenotype conversion of smooth muscle cells, contributing to the formation of atherosclerotic plaque.

Figure 8. The schematic diagram shows the process of fibrin deposition, macrophage infiltration and atherosclerosis formation. Stage I: Hypertonicity → NFAT5-dependent PAI-1 gene transcription → PAI-1 secretion. Stage II: PAI-1 secretion → Antifibrinolytic activation/adhesive molecules → Fibrin deposition/monocytes adhesion and infiltration. Stage III: Endothelial dysfunction leads to fibrin deposition, macrophage-driven foam cells and phenotype conversion of smooth muscle cells, contributing to the formation of atherosclerotic plaque.