Inflammation: The Pathological Axis of Cisplatin-Induced Renal Injury - PubMed
8 hours ago
- #Innate Immunity
- #Cisplatin Nephrotoxicity
- #Macrophage Polarization
- Cisplatin-induced acute kidney injury (CI-AKI) is a major dose-limiting side effect of chemotherapy.
- Cisplatin accumulates in renal tubular epithelial cells (RTECs) via transporters OCT2 and CTR1, causing mitochondrial damage and ROS production.
- Damage-associated molecular patterns (DAMPs) released from RTECs activate innate immune pathways like TLR4/MyD88/NF-κB and NLRP3 inflammasome, driving inflammation.
- Macrophages play a dual role: early M1 polarization worsens tubular injury, while later M2-like macrophages help resolve inflammation and promote tissue repair.
- Targeting inflammation through TLR4/NF-κB inhibition or modulating macrophage polarization may offer renoprotective strategies without reducing cisplatin's anticancer effects.