ACSL4 and liver dysplastic nodule: Simultaneously, the disruption of system Xc function during ferroptosis prevents GPX4 from performing its normal antioxidant function (3), and activation of the Hippo pathway induces the upregulation of ACSL4 expression, leading to increased lipid peroxidation (34) and exacerbation of oxidative damage in the kidneys in DN; this may be a potential mechanism by which iron metabolism and ferroptosis promote the development and progression of DN.