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however, this response was blunted compared to normal subjects, despite higher plasma IGF-1 concentrations, indicating partial resistance in advanced CKD.67 This reduced response is likely due to a decrease in the distribution and shortened half-life of the IGF-1 in dialysis patients.68 Furthermore, resistance to the GH-mediated bioactive IGF-1 stimulation has been demonstrated in non-diabetic hemodialysis patients, suggesting the presence of additional inhibitory mechanisms.69 In predialysis patients, increased production of IGFBPs has been observed, which may bind free IGF-1 and contribute to the attenuation of its renal effects.70 Therefore, as previously mentioned, elevated levels of renal IGFBPs in conditions of renal insufficiency may act as inhibitors of IGF-1 contributing to resistance in the proximal tubular cells.4 On the other hand, the renal anabolic actions of IGF-1 can be detrimental in the context of polycystic kidney disease (PKD), as it promotes renal cell proliferation and kidney enlargement

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787 Ferroptosis has been shown to be associated with the pathological mechanism of SCIRI, and Fer-1 inhibits ferroptosis of spinal neurons in rats through the ERK1/2/SP1/GPX4 signaling pathway, improving nerve function after SCIRI