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1 To date, multiple mechanisms of tissue damage have been implicated in SLE, including oxidative stress and free radicals, fibrosis, complement-mediated pathways, and a panoply of enzymatic cascades including matrix metalloproteinases, the renin-angiotensin system, plasmin, and kallikreins

These disease-associated adipocytes release lipids, hormones, adipokines and tumor-promoting factors that facilitate tumor growth and metastatic progression (90)

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Several challenges continue to hinder the clinical application of Exos in ferroptosis-related conditions