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Journal of Community Hospital Internal Medicine Perspectives

LOX-1 activation further induces ROS production, promotes ox-LDL uptake, reduces NO release from endothelial cells, induces the expression of ET-1, AT1 receptors and cell adhesion molecules, and enhances vascular homeostasis disorders and endothelial dysfunction [61]

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Tumor microenvironmental signals triggered ATF4-mediated activation of PHGDH, leading to a redox-dependent mechanism that regulated tumor overgrowth

Upregulation of the glucocorticoid receptor (GR) [3], as well as ligand-independent AR activation, promote ADT resistance [1]
