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Iron accumulation, lipid peroxidation, and decreased GPX4 expression, which are characteristic hallmarks of ferroptosis, contribute to inflammation through the induction of oxidative stress and the activation of the high mobility group box-1 protein1-advanced glycosylation end-product-specific receptor signaling pathway and extracellular signal-regulated kinase, respectively [77,78,79]

Biol Res 42:315326 Sasaki-Sekimoto Y, Taki N, Obayashi T, Aono M, Matsumoto F, Sakurai N, Suzuki H, Hirai MY, Noji M, Saito K, Masuda T, Takamiya K, Shibata D, Ohta H (2005) Coordinated activation of metabolic pathways for antioxidants and defence compounds by jasmonates and their roles in stress tolerance in Arabidopsis

This non-specific action can also interfere with the physiological signaling roles of ROS (as discussed in Section 2.2), potentially leading to unintended adverse effects or a lack of targeted efficacy

Recent reports indicate a more complex mechanism in which wild-type p53 may enhance survival advantage by promoting antioxidation in some cases, and p53-mediated activation of p21 (encoded by CDKN1a) inhibits phospholipid oxidation by protecting intracellular mercaptans (including GSH) (Tarangelo et al., 2018

Excessive ROS can be reduced by cellular antioxidant systems, such as the Nrf2-mediated antioxidant system, GSH, and NADPH [18, 19]

In APCs, the MyD88-dependent pathway regulates cell maturation, characterized by the increased expression of CD80, CD86, MHC class II, and inflammatory cytokines, e.g., TNF, interleukin (IL)-6, and IL-12