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The role of oxidative stress in the development of MCS is now widely accepted, along with alterations in redox status that contribute to chronic mild systemic inflammation

Reduction of Stromal Fibroblast-Induced Mammary Tumor Growth, by Retroviral Ribozyme Transgenes to Hepatocyte Growth Factor/scatter Factor and its Receptor, C-MET

Thus, macrophage ferroptosis and macrophage-derived foam cell ferroptosis persist throughout plaque formation and progression to advanced unstable plaques

High levels are less common and typically stem from underlying medical conditions, such as liver disease, leukemia, or systemic lupus erythematosus (SLE)