The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.

Ferroptosis represents a distinctive mechanism of cell death, differing from necroptosis, necrosis, and apoptosis. It is triggered by the accumulation of lipid peroxides, driven by iron-catalyzed reactions. This oxidative damage is essential for triggering the ferroptotic pathway. Compared with apoptosis and necroptosis, ferroptosis is activated earlier in acute kidney injury (AKI), serving as a preemptive mechanism of cell death. Ferroptosis acts as a link between synchronous waves of renal tubular cell death by triggering cell death amplification loops and connects cell damage with inflammatory responses, thus constituting a crucial stage in the progression of AKI. This paper discusses the mechanisms that trigger ferroptosis in AKI and how ferroptosis, as a preemptive mode of cell death, exacerbates AKI through ferroptotic waves, modulates inflammatory responses, triggering apoptosis, necroptosis, and pyroptosis.