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P.et al (2001)

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This nephrotoxic moiety additionally activates aryl hydrocarbon receptor (AhR) signaling architectures within podocyte and mesangial cellular compartments, inducing CYP1A1 expression paradigms while exacerbating oxidative stress microenvironments and promoting TGF-1 transcriptional upregulation, thereby exponentially accelerating glomerulosclerotic progression and tubulointerstitial fibrotic transformation trajectories (Iwashima et al., 2024