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according to the current paradigm, TIMP-2 first forms a complex with proMMP-2 by binding to its hemopexin domain, after which the complex localizes onto the cell surface where it binds to the active site of an MT1-MMP molecule, forming a ternary complex which permits the activation of proMMP-2 by another free MT1-MMP [85,87]
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4.2 Lipid peroxidation and oxidative stress in RA Oxidative stress as a major pathogenic hallmark of RA promotes the local microenvironment at the RA lesion sites, enhances abnormal synoviocytes proliferation, and exacerbates inflammatory infiltration (42, 43)
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