SUMMARY
The authors hypothesized that CX3CL1 deficiency could mitigate ferroptosis, reducing cisplatin-triggered podocyte injury and kidney inflammation. Mechanistically, CX3CL1 deficiency prevented mitochondrial dysfunction, mitigated endoplasmic_reticulum (ER) stress, inhibited the HIF1A/HO-1 pathway, and protected against Cis-AKI by suppressing ferroptosis in podocytes. Lentiviral_vector UbiMCS-CBh-gcGFP-IRES-Puro-CX3CL1 was employed to induce CX3CL1 knockdown (CX3CL1-KD) in podocytes, following the manufacturer`s instructions from Shanghai Genechem Co. Ltd Three distinct podocyte groups were established: the control group, the cisplatin-treated group (20 μM/ml, 24 h), and the CX3CL1KD + cisplatin group. The investigation revealed elevated . . .
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