FTH1 and acute kidney injury: In the proximal tubules, the specific absence of FTH exacerbates AKI induced by rhabdomyolysis or cisplatin, reducing the survival rate in mice.[83] In contrast, inducing the expression of FTH in the kidney can mitigate renal injury by enhancing iron chelation within ferritin, reducing oxidative stress markers, and alleviating the decline in renal function caused by ischemia‐reperfusion, demonstrating a protective effect in AKI mouse models.[83, 102]