FGF4 alleviates renal injury caused by ischemia-reperfusion(I/R) by inhibiting ferroptosis and pyroptosis

Renal ischemia-reperfusion injury can lead to severe renal function impairment, manifested by a significant increase in serum creatinine, renal tubular obstruction, and even necrosis, which can lead to acute renal failure. This injury can also trigger systemic inflammatory response syndrome and even lead to multiple organ dysfunction. It poses a serious threat to the life and health of patients, so it is urgent to find potential drugs for treatment. In our current work, we evaluated the effects of FGFs on kidney injury caused by ischemia-reperfusion. We first established a model of kidney cell injury caused by ischemia-reperfusion. The biological functions of FGFs were further evaluated through a series of biochemical techniques. The experimental data showed that, FGFs can effectively improve the damage of kidney cells caused by ischemia-reperfusion. FGFs can alleviate iron death and pyroptosis of kidney cells caused by ischemia-reperfusion. Further work showed that FGF4 also alleviated inflammation and oxidative stress damage caused by ischemia-reperfusion. Mechanism research also showed that FGFs effectively alleviated ischemia-reperfusion-induced kidney injury by activating AMPK-mediated signaling pathways. Furthermore, in vivo, we also found that FGF4 can effectively alleviate the kidney ischemia-reperfusion injury. This finding not only indicates the potential therapeutic prospects of FGF4 for ischemic diseases, but also provides a new pharmacological target for the treatment of renal ischemia-reperfusion injury.