TXN and arteriosclerosis disorder: This therapeutic mechanism involved the injection of recombinant Trx into mice, inducing the activation of mitogen-activated protein kinase 4 in endothelial cells, which in turn reduced the activity of the transforming growth factor-β (TGFβ)-matrix metalloproteinase-2- TGFβ receptor II pathway, decreased the aggregation of extracellular matrix protein disulfide bonds, and mitigated the progression of arteriosclerosis, providing a transient therapeutic effect on hypertension [72].