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It inhibits GPX4, leading to tumor-specific ferroptosis, and TA is used to chemically reduce Fe 3+ to Fe 2+ and continuously supply Fe 2+ to maintain the iron redox cycle and maintain the Fenton reaction [201]

Our findings indicated that targeting ACSL4 or, alternatively, upregulating GPX4 or FSP1 may help mitigate AKI by reducing ferroptosis, offering potential therapeutic strategies for oxalate-induced AKI

Once activated, they express -smooth muscle actin (-SMA) and synthesize collagen, as well as other extracellular matrix proteins, such as fibronectin [11]

Rosenkranz E, Maywald M, Hilgers RD, Brieger A, Clarner T, Kipp M, et al