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At the pathogenic level, PsO and PsA share core inflammatory mechanisms driven by dysregulation of the IL17/IL23 and Tumour Necrosis Factor (TNF)- cytokine axes (14), contributing to keratinocyte hyperproliferation, synovial inflammation, and enthesial disease (1518)

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This process is similar to the mechanism of ferroptosis, where ROS generation is intensified, causing oxidative damage that can exacerbate adriamycin-induced cardiotoxicity

Melanoma Res 27 (3): 258-267, 2017

doi: 10.1172/JCI78371

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