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In the complex landscape of CKD, characterized by heightened inflammation, oxidative stress, leukocyte migration, adhesion, cell death, and the emergence of a thrombotic phenotype, an array of circulating molecules holds sway over endothelial equilibrium These molecules exert their influence through frequently activated cellular signaling pathways, including ROS, MAPK/NF-B, Aryl-Hydrocarbon Receptor, and RAGE pathways (70)

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