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For example, the tumor suppressor p53 and the nuclear factor erythroid 2-related factor 2 (Nrf2) have been shown to modulate ferroptotic cell death through their effects on lipid peroxidation and antioxidant defense

The E-cadherinMerlinHippoYAP axis has been shown to control ACSL4 transcription, thereby linking cellcell contact signaling to ferroptosis susceptibility [93], and further supporting ACSL4 as a pivotal mediator of ferroptotic regulation [94]

Following reconstitution, it is advisable to aliquot the extract into multiple tubes and avoid repeated freezethaw cycles to retain its stability and functional integrity

In recent years, epigenetic regulation has emerged as a central mechanism linking these pathological processes, mediating persistent alterations in gene expression during DKD progression [6, 7]